The keystone is the sphenoid bone; all neurovascular structures to the orbit pass through this bone. The superior orbital fissure is the space between the lesser wing and the greater wing of the sphenoid bone. The optic canal is medial to the superior orbital fissure within the lesser wing.
Medial Orbital Wall
The medial wall comprises four bones: the maxillary, lacrimal, ethmoid, and sphenoid bones. The medial wall is the thinnest of the four orbital walls, appropriately termed the lamina papyracea, measuring only 0.2 to 0.4 mm in thickness. Though the medial wall is the thinnest orbital wall, it is the floor that is most frequently fractured. This is attributed to the perpendicular septa of the ethmoid sinus that reinforce the lamina papyracea.
The anterior lacrimal crest is located in the frontal process of the maxilla, whereas the posterior lacrimal crest is formed by the lacrimal bone. Between these crests lies the fossa for the lacrimal sac. The anterior and posterior lacrimal crests also form attachments to the anterior and posterior limbs of the medial canthal tendon, respectively.
Superiorly, the ethmoid bone joins the orbital roof at the frontoethmoidal suture line, a useful surgical landmark. It denotes the level of the cribriform plate, which indicates the roof of the ethmoid sinus and the floor of the anterior cranial fossa. The anterior and posterior ethmoidal foramina are located within the frontoethmoidal suture line. The anterior ethmoidal foramen transmits the anterior ethmoidal artery and nerve branches of the nasociliary nerve, which innervates the anterior ethmoidal air cells, mucosa of the upper nose, and the nasal tip. The posterior ethmoidal foramen conveys the posterior ethmoidal artery and a sphenoethmoidal nerve branch from the nasociliary nerve that supplies the posterior ethmoidal air cells, anterior cranial fossa dura, and upper nasal mucosa. Injury to the ethmoidal arteries can cause excessive bleeding during orbital surgery. Furthermore, the locations of these foramina identify relative distances along the medial orbital wall toward the optic canal. The anterior ethmoidal foramen is located 20 to 24 mm posterior to the anterior lacrimal crest, the posterior ethmoidal foramen 12 mm behind this, and the optic canal a further 6 mm posterior to this (Fig. 34.1B). These distances can be recalled using the mnemonic “24-12-6.”
Behind the ethmoid bone and forming the posterior portion of the medial wall is the body of the sphenoid bone. The sphenoid sinus lies between the two orbital apices. The optic canal is situated in the superonasal portion of the apex and is enclosed by the body of the sphenoid medially, the lesser sphenoid wing superiorly, and the optic strut inferotemporally.
The orbital floor shows the greatest degrees of deformation with static loading of any of the orbital walls, which explains the high rate of floor fractures associated with blunt trauma. The orbital floor measures 0.5 to 1 mm in thickness, with its thinnest point located medial to the infraorbital canal. This portion of the floor is most commonly damaged in orbital blowout fractures, often resulting in injury to the infraorbital nerve and causing anesthesia of the cheek, upper lip, and upper canines. The infraorbital nerve may be exposed in the case of a fracture, and care must be taken to preserve it during surgical dissection.
The inferior oblique muscle originates along the anteronasal aspect of the orbital floor just lateral to the lacrimal fossa. It can be safely elevated in a subperiosteal plane when approaching combined medial wall and floor fractures (Fig. 34.1C).
Lateral Orbital Wall
The lateral orbital wall is the strongest orbital wall. It is characterized by variable thickness along the course of the rim and wall. The width of the lateral orbital rim at the canthal level is 1.0 to 1.1 cm and is thinner as it approaches the frontozygomatic suture and lacrimal gland fossa superiorly. The frontozygomatic suture often separates in the setting of zygomaticomaxillary fractures. Below the level of the canthus, the width of the rim is 1.3 to 1.5 cm. The thinnest portion of the wall is located at the zygomaticosphenoid suture, 1 cm behind the orbital rim. During lateral orbitotomy surgery, removing the lateral orbital rim down to this thinner portion of the zygomatic bone allows for the creation of a bone window, providing decompression of orbital contents and access to the intraconal space (Fig. 34.1D). Approximately 1 cm posterior to the zygomaticosphenoid suture, the sphenoid bone thickens into a trigone and subsequently becomes thinner near the superior orbital fissure, approximately 2.2 cm from the rim.
A small, bony promontory located 11 mm inferior to the frontozygomatic suture can be found just within the orbital rim. This important surgical landmark, Whitnall’s tubercle, is the point of attachment for several structures, including the lateral canthal tendon, the check ligament for the lateral rectus, Lockwood’s suspensory ligament, and the lateral horn of the levator aponeurosis. At the anterior end of the inferior orbital fissure, a small groove may be noted for the passage of the zygomatic nerve and vessels. The groove often develops into a canal, which divides within bone to conduct the zygomaticofacial vessels and nerves onto the malar eminence and face and the zygomaticotemporal vessels and nerves into the temporal fossa. These neurovascular bundles are often encountered in lateral orbitotomy surgery and in operative repair of zygomatic fractures (Fig. 34.1E).
Orbital Roof and Optic Canal
The frontal bone and lesser wing of the sphenoid comprise the orbital roof. At the orbital apex, the lesser wing of the sphenoid contains the optic canal, which is 5 to 6 mm in diameter and 10 to 12 mm in length. The optic nerve and ophthalmic artery pass through the optic canal and into the intraconal space through the annulus of Zinn. It is bounded medially by the body of the sphenoid bone, superiorly by the lesser wing of the sphenoid, inferolaterally by the optic strut, and laterally by the anterior clinoid process (Fig. 34.1F).
For approximately 10 mm of its length, the optic nerve is fixed and enclosed within the optic canal, which contributes to the vulnerability of the nerve in this location. Trauma to the optic nerve can be direct or, more often, indirect. In the latter case, the mechanism of traumatic optic nerve injury involves the transmission of trauma to the optic nerve through the orbit to the bony optic canal, which can lead to contusion of the nerve or shearing of the pial vessels and subsequent infarction. Direct optic neuropathy is caused by a direct fracture in the canal, a bony segment impinging on the nerve, or a foreign body directly damaging the nerve.
The frontal sinus is located within the frontal bone in the anteromedial portion of the roof. The size of this sinus is extremely variable, and in some individuals, it may extend as far laterally as the lacrimal gland fossa and as far posteriorly as the optic canal. Orbital roof fractures are more common in young children, who have not yet developed pneumatized frontal sinuses, and these fractures are more likely to involve intracranial injury. Frontal trauma in older patients tends to be absorbed by the frontal sinus, thereby preventing extension to the orbital roof.
The orbital septum is a multilayered fibrous plane that marks the anterior boundary of the orbit. Peripherally, it attaches to the periosteum of the orbital rims at the arcus marginalis, and centrally, it joins the lid retractors at the lid margins (Fig. 34.1F). Laterally, it attaches 1.5 mm anterior to the lateral orbital tubercle and medially it passes anterior to the trochlea and follows the posterior lacrimal crest, in front of the medial check ligament and behind the lacrimal sac.
Knowledge and understanding of the orbital septum is vital to the orbital and eyelid surgeon. It limits superficial infection from spreading deeper into the orbit, and direct traumatic disruption of the orbital septum can allow passage of pathogens and foreign materials into the orbital soft tissue (see Chapter 10).
Orbital Hemorrhage and Compartment Syndrome
Bounded posteriorly by contiguous bony walls and anteriorly by the fibrous septum, the orbit is an enclosed space with limited ability to expand. Orbital compartment syndrome occurs when a rapidly developing intraorbital process, such as hemorrhage, air (pneumo-orbitum), retrobulbar injection, inflammation, tumor, or abscess results in an acute rise in orbital tension (Fig. 34.2). Less commonly, massive fluid resuscitation after a burn injury can lead to orbital compartment syndrome. Even a small collection of fluid may impede venous drainage and cause a dramatic rise in orbital pressure. This is a true ocular emergency requiring prompt recognition and intervention to avoid permanent visual loss.
In a review published in 2009, Lima et al. attributed 64% of cases of orbital compartment syndrome to orbital hemorrhage from various causes, including trauma, surgery, and other underlying medical conditions.11
As in compartment syndrome elsewhere in the body, increased tissue pressure in an enclosed space rapidly leads to decreased perfusion. The mechanism of visual loss may be direct compressive optic neuropathy, optic nerve ischemia from compression or stretching of optic nerve vasculature, optic nerve stretch from marked anterior globe displacement, or retinal ischemia from central retinal artery occlusion.12 Because there is no lymphatic drainage in the orbit, the only outflow pathway is through the superior and inferior ophthalmic veins, which may be compromised from increased intraorbital pressure as well.
Acute proptosis associated with lid edema, conjunctival chemosis, and visual disturbances may also be seen with orbital inflammation, thyroid ophthalmopathy, ruptured dermoid cyst, and enlarging intraorbital masses. The clinical course of these entities tends to be much slower compared with that of traumatic orbital compartment syndrome.
The cardinal signs of optic nerve evaluation include visual acuity, color vision, pupillary reactions, and visual field examination. Combining these with measurement of intraocular pressure, extraocular motility, exophthalmometry, and palpation forms a comprehensive orbital examination. In the case of orbital compartment syndrome, there may be decreased visual acuity, afferent pupillary defect, and elevated intraocular pressure. Orbital signs include limited extraocular movements and proptosis, with increased resistance to retropulsion of the globe. Periocular edema and ecchymosis may be present. Funduscopy may reveal optic disk edema, retinal venous congestion, retinal artery occlusion, and/or retinal edema.
Early recognition and immediate management is essential to prevent visual loss, as 60 to 100 minutes of sustained raised orbital pressure can produce irreversible visual loss.13 Measures to reduce orbital and ocular pressure should be taken on the basis of clinical indications and should never be delayed while waiting for the results of radiographic studies.
Intraocular pressure (IOP) is a good indication of orbital tension.14 With IOP less than 40 millimeters of mercury (mm Hg), presence of ocular movements, no afferent pupillary defect, and preservation of visual acuity, it is adequate to institute close observation with monitoring of vision, ocular movements, and IOP. Medical interventions can also be initiated in these cases, and elevated IOP can be treated with a combination of topical β-blocker, carbonic anhydrase inhibitor, prostaglandin analog, or α-agonist therapy and systemic osmotic agents and/or carbonic anhydrase inhibitors. Intravenous mannitol and oral glycerin are the most commonly used systemic hyperosmotic agents. Mannitol can be administered at a dose of 1.5 to 2.0 g/kg as a 20% solution over a period as short as 30 minutes. Oral glycerin is available in a 50% solution (Osmoglyn). The initial oral dose is 1 to 1.5 mg/kg, taken as a single dose. Isosorbide 40% may be substituted for glycerin in patients with diabetes, as this agent is not metabolized by the body and should not raise blood glucose levels. Available systemic carbonic anhydrase inhibitors include oral (500 mg, sustained release, orally twice daily; or 250 mg, orally four times daily) or intravenous acetazolamide and oral methazolamide (25–50 mg orally three times daily).
There are specific indications for advancing from medical to surgical therapy to lower intraorbital pressure more rapidly and restore visual function. An IOP higher than 40 mm Hg with a tense orbit, any evidence of visual loss, or an afferent pupillary defect warrants urgent lateral canthotomy and cantholysis.15 It is important to completely transect the inferior limb of the lateral canthal tendon (inferior cantholysis) to achieve adequate decompression. This typically results in an immediate decrease in intraorbital pressure and resumption of blood flow. If necessary, the septum may be released by cutting its insertion close to the bony rim, or a superior cantholysis may also be performed. The resultant wound can be left to heal by secondary intention or can be repaired at a later time. If orbital compartment syndrome is caused by an expanding hematoma or trapped air, percutaneous aspiration may be necessary.16,17 If compartment syndrome is primarily attributed to infection and there is concern about orbital abscess formation, prompt initiation of intravenous antibiotics and orbitotomy with evacuation of the abscess and placement of a percutaneous drain should be considered.
Patients should avoid coughing, straining, and nose blowing.18 Cough suppressants, antiemetics, and stool softeners should be considered. The head of the bed should be elevated, and blood pressure and coagulopathies should be normalized. If the septum has been violated, systemic prophylactic antibiotics should be considered. Likewise, intravenous or oral corticosteroids can be started to control inflammation.
Direct and Indirect Optic Neuropathy
The optic nerve is sensitive to both direct and indirect trauma. Examples of direct trauma to the optic nerve include avulsion, transection, compression, or stretching. In optic nerve avulsion, the nerve is forcibly disinserted from the retina, choroid, and sclera. Several mechanisms of optic nerve avulsion have been postulated, including sudden extreme rotation of the globe, sudden rise in IOP leading to the expulsion of nerve out of scleral canal, and sudden anterior displacement of the globe. The resulting blindness is permanent. Partial or complete transection of the optic nerve may occur from knife or bullet wounds, bone shards, or other penetrating foreign bodies (Fig. 34.3). The entry wound may be inconspicuous, but imaging confirms the diagnosis. Visual loss is typically irreversible. Direct compression of the optic nerve may result from optic nerve sheath hematoma, foreign bodies or bone fragments, or raised orbital pressure from orbital compartment syndrome. Stretch of the optic nerve may be caused by severe proptosis from diffuse orbital edema or hemorrhage or from displacement of the globe from a foreign body or displaced bone segments. Significant tenting of the posterior globe is associated with a poor visual prognosis.
Indirect traumatic optic neuropathy can also produce profound visual consequences. The presumed mechanism includes shearing of axons within the optic nerve or microvasculature supplying the optic nerve, resulting in immediate ischemia from vascular insufficiency.21 A secondary mechanism results in further damage to the optic nerve axons from trauma-induced edema within the optic canal. Therefore, in up to 10% of these cases, visual loss can present in a delayed manner.22 Treatment with surgery and/or high-dose steroids is intended to minimize this secondary injury.
The differential diagnosis of optic disk edema includes papilledema, retinal vein occlusion, optic neuritis, anterior ischemic optic neuropathy, compressive optic neuropathy, infiltrative optic neuropathy, and diabetic optic neuropathy.
TON presents with vision loss, color vision desaturation, visual field defects, and afferent pupillary defect. In unconscious patients, both pupil assessment and flash visual evoked potentials may help assess optic nerve function. Optic disk hemorrhage or edema in the acute setting may evolve into optic atrophy. In optic nerve avulsion, funduscopy confirms an absent disk with surrounding retinal hemorrhage. Presenting symptoms and signs associated with poor visual prognosis include no light perception vision,23 afferent pupillary defect exceeding 2.1 log units,24 and flash visual evoked potentials with amplitude less than 50% of the unaffected side.25
Treatment of direct traumatic optic neuropathy can include optic nerve fenestration; drainage of surrounding blood, fluid, or air; removal of foreign material; or bony decompression. However, treatment of indirect traumatic optic neuropathy is controversial because the natural history is highly variable, with up to 30% of affected adults spontaneously recovering some vision,26 often weeks later. In the 1980s, high-dose corticosteroids were favored, especially in cases of documented progressive vision loss. This was based on National Acute Spinal Cord Injury Studies27,28: an initial dose of intravenous methylprednisolone 30 mg/kg was followed by an infusion of 5.4 mg/kg/h for 24 hours and was found to result in better recovery if administered within 8 hours of the injury. However, treatment delayed beyond 8 hours was thought to be detrimental. Several authors have reported visual recovery following optic canal bone decompression from transcranial or endoscopic transsinus approaches. The International Optic Nerve Trauma Study,22 published in 1999, found no significant differences in outcomes in the steroid, surgical, and nontreatment groups. Furthermore, in 2004, the Corticosteroid Randomization After Significant Head Injury (CRASH) trial29 found a correlation between high-dose methylprednisolone and increased mortality in patients with concomitant head trauma. Therefore, given the morbidity of surgery and the potential side effects of high-dose steroids, many clinicians now avoid surgery and restrict the use of corticosteroids to cases of optic neuropathy without intracranial injury, and only if they are administered within 8 hours of the onset of visual loss.
Orbital Foreign Bodies
An intraorbital foreign body (IOFB) should be considered in any case of penetrating orbital trauma or unexplained posttraumatic orbital inflammation or infection. In one large study of 2060 eyes (1971 patients) who sustained ocular injuries severe enough to require hospital admission, foreign bodies were encountered in the eye or orbit in 10.2% of the eyes.30 The vast majority of affected patients are male and under the age of 30 years. Metallic foreign bodies are encountered more commonly compared with organic or glass foreign bodies.31
Classically, the common causes of IOFBs are work-related accidents, recreation or motor vehicle collisions, assaults, and self-inflicted injuries. Of these, the most common cause is hammering metal on metal, responsible for 60% to 80% of cases. However, IOFBs may occur even during relatively trivial trauma.