Fig. 9.1
Bones of the right orbit A Frontal, B Ethmoid, C Lacrimal, D Maxillary, E Greater wing of sphenoid, F Zygoma, G Palatine, H Lesser wing of sphenoid
The orbit contains the optic nerve (II), the globe, orbital fat, the extraocular muscles and their corresponding innervating nerves [oculomotor (III), trochlear (IV), abducens (VI)], trigeminal nerve (V2), blood vessels and nerves, and the lacrimal gland. The greater and the lesser wing of sphenoid form the superior orbital fissure. The superior orbital fissure transmits cranial nerves III, IV, VI, and the ophthalmic division of trigeminal nerve (V1), superior orbital vein, and sympathetic fibers. The inferior orbital fissure lies between the lateral orbital wall and the floor of the orbit. It transmits V2, the zygomatic nerve, and inferior ophthalmic vein. The optic canal is located in the lesser wing of sphenoid and is approximately 8–10 mm long. It transmits the optic nerve, ophthalmic artery, and sympathetic nerve fibers. Traumatic fracture of the optic canal can result in optic nerve damage and vision loss. The paranasal sinuses are located just outside the orbit (Fig. 9.2).
Fig. 9.2
Axial (a) and coronal (b) orbital CT showing relationship of sinuses to orbit: A Ethmoid sinus, B Zygoma, C Greater wing of sphenoid, D Sphenoid sinus, E Maxillary sinus. F Frontal bone
The annulus of zinn is an important anatomical landmark of the orbit formed by the common origin of the superior, inferior, medial and lateral rectus muscles. The optic foramen and the central portion of the superior orbital fissure are enclosed within the annulus. This part of the orbital apex is called the oculomotor foramen. The superior and inferior divisions of CN III, CN VI, and the nasociliary branch of CN V pass through this foramen (Fig. 9.3). The lacrimal, frontal and trochlear nerve and the superior ophthalmic vein pass through the superior part of the fissure outside the annulus.
Fig. 9.3
Structures passing through the right orbital apex and superior orbital fissure: A Lacrimal nerve, B Frontal nerve, C Trochlear nerve (CN IV), D Superior ophthalmic vein, E Superior division of oculomoter nerve (CN III), F Abducen nerve (CN VI), G nasociliary nerve, H Inferior division of CN III, I Optic nerve, J Ophthalmic artery
The orbit is divided into different compartments by virtue of the location of the extraocular muscles, periorbita (periosteum lining the orbital bones), and the tenons fascia that form five surgical spaces within the orbit. The extraconal space lies between the periorbita and rectus muscle cone. The intraconal space lies within the rectus muscle cone. The subperiosteal space lies between bone and periorbita. The episcleral space lies between Tenon’s capsule and the globe. Lastly, the subarachnoid space lies between the optic nerve and the optic nerve sheath (Fig. 9.4). The optic nerve is within the intraconal space. Any traumatic event that causes a compartment syndrome, either due to accumulation of air or blood within the intraconal space, poses a risk for optic nerve compression and possible long-term vision loss. The intermuscular septum is a membranous ring that connects the rectus muscles in the anterior portion of the orbit. This ring divides the orbit into intraconal and extraconal compartments.
Fig. 9.4
a Axial and b Cornonal view of the orbital spaces: A Extraconal space, B Intraconal space, C Sub Tenon space, D Subarachnoid space, E Extraocular Muscle, F Subperiosteal space
The orbital blood supply arises primarily from the ophthalmic artery, a branch of the internal carotid artery. A small portion of the supply is also derived from the internal maxillary and facial arteries which are branches of the external carotid artery. The venous drainage for the orbit is provided mainly by the superior ophthalmic vein. The vein runs from the superonasal quadrant of the orbit, through the superior orbital fissure draining into the cavernous sinus.
Orbital Trauma
Evaluation
A detailed history and examination is essential to guide the clinician in determining the extent of trauma and potential need for emergent surgical intervention to prevent long-term morbidity including permanent visual loss [1]. It is important to ascertain the timing and mechanism of trauma, and blunt versus penetrating mechanisms. Changes in visual acuity or double vision, if present, provide a valuable clue that the injury to the globe or orbit may be of a serious nature. Their absence, however, does not rule out the potential for severe trauma. Nausea or vomiting in the setting of a suspected orbital wall fracture is highly suspicious of possible muscle entrapment, which is an ocular emergency. Examination of a patient with orbital trauma involves careful evaluation of visual acuity and extraocular movements in all cardinal positions of gaze. Confrontation visual fields can be valuable to determine the presence of optic nerve trauma. Once a ruptured globe has been ruled out, intraocular pressure should be assessed in a standard fashion.
Imaging
Orbital CT without contrast is a useful study for a quick evaluation of pathology and is the standard imaging modality used in the setting of trauma. It exposes the patient to a low dose of radiation (1–14 mSv) [2]. Coronal sections are best for evaluating orbital fractures. CT is also the study of choice when an orbital or intraocular foreign body is suspected [3].
MRI allows better visualization of the orbital soft tissue, does not involve radiation exposure, but is contraindicated if a metallic foreign body is a possibility, and is rarely used in traumatic patients in the acute setting.
Different Presentations of Orbital Trauma
- 1.
Orbital Contusion:
Orbital contusion occurs secondary to blunt trauma and can present with variable amounts of pain, blurry vision, proptosis, periorbital edema and ecchymosis. Radiography shows preseptal edema in the absence of fractures and other signs of severe injury. Treatment is typically conservative and consists of elevation of the head of the bed and cold compresses, and analgesics as needed. Some advocate the use of oral steroids to alleviate swelling and inflammation. In most cases the signs and symptoms are self-limiting and resolve within days to weeks.
- 2.
Orbital Fractures:
Orbital blowout fractures account for 18–50% of all maxillofacial trauma [4]. Common presenting signs in patients with blowout fractures include periocular edema and ecchymosis, diplopia with decreased extraocular movements, and hypoesthesia. Large orbital fractures can sometimes lead to noticeable enophthalmos (>2 mm) once the initial periorbital edema subsides. Thin-cut orbital CT, especially coronal sections, is essential to investigate the extent of the fracture.
Orbital Floor Fracture
Orbital floor fractures account for 65–80% of all orbital fractures. Fractures are classified as either “Pure” or “Impure”. The more common pure fractures have no rim involvement and are caused by blunt impact on the globe causing secondary fracture of the floor via retropulsion. The less common impure fractures are caused by direct impact to the rim causing fracture of the rim and floor via buckling.
Two theories predominate to describe the pathophysiology of an orbital blowout fracture: the hydraulic or retropulsion, and the buckling theories. The hydraulic theory suggests trauma, with a significant impact to the globe, results in a retropulsion force that results in a blow out fracture [5–7]. In the buckling theory, traumatic forces are conducted along the orbital rim to the orbital bones resulting in fracture [5–7].
Patients with an orbital fracture may present with edema, ecchymosis, enophthalmos, and diplopia. It is important to palpate the area for any crepitus, or bony step off of the orbital rim if a displaced fracture is present [8]. Extraocular movements may be limited due to chemosis, orbital hemorrhage or inflammation, muscle or nerve trauma. Floor fractures involving the infraorbital canal can result in numbness of the V2 distribution including the cheek, lower eyelid, upper lip, upper gums, and teeth on the affected side. This typically resolves over weeks to months of observation. Patients can present with limitation of both supra- and infraduction with diplopia in up- and/or down gaze. If the fracture site is large, typically more than 50% of the entire floor and especially when in conjunction with large medial wall fractures, it may cause enophthalmos due to herniation of orbital soft tissues into the adjacent sinuses. The great majority of orbital floor fractures do not require surgical intervention.
Entrapment is more commonly seen in trapdoor, orbital floor fractures in the pediatric population due to higher elasticity of bones in the younger population. Orbital bones in children are more elastic and tend to instantly snap back into normal position after trauma, hence allowing the trapping of orbital soft tissues within the fracture plane. Patients may present with nausea, vomiting, diplopia, and bradycardia. This should be suspected when there is restriction of globe movements in both supra- and infraduction, often with the globe failing to elevate vertically past the midline. Globe movement, in acute trauma, maybe limited due to muscle trauma, hematoma, edema, or pain. True entrapment can be confirmed by clinical exam, and careful review of radiography. In the authors’ experience, radiologists may at times miss an entrapped fracture and the CT findings can be subtle. It is therefore paramount for surgeons to carefully review thin cut CT imaging of all orbital trauma patients. If an entrapped fracture is suspected, the patient must be placed on cardiac monitoring and instructed to relax without extreme eye movements, which may trigger the oculocardiac reflex, with urgent preparation for surgical repair. The oculocardiac reflex, a reflex arc of the trigeminal and vagus nerves, can cause bradycardia or cardiac arrhythmia in patients with an entrapped orbital fracture [3, 9–12].
Figure 9.5 depicts a schematic of an entrapped floor fracture detailing the complex network of fascia that exists in the orbit and that has an intimate relationship with the inferior rectus muscle. It is important to note that an entrapped fracture can result from the incarceration of any orbital soft tissue including the fat, and does not require the inferior rectus muscle being at or inferior to the plane of the fracture. It is this fascial network that is a key in making the orbital soft tissues a single functional unit.
Fig. 9.5
Schematic of a right orbital floor fracture with entrapment (Courtesy Sunny Tang). A–D. Extraocular muscles, E entrapped soft tissue, F Fascia
The maxilla in the posteromedial aspect of the orbital floor is the thinnest part of the floor and commonly the site of fractures (Fig. 9.6). Rarely an orbital fracture may present as a “white-eyed blowout” fracture especially in children under the age of 16 [13]. Patients with these kinds of fractures show minimal signs of soft tissue injury, minimal enophthalmos, and minimal prolapsed tissue or fracture area on CT scans. However, they do show marked restriction in both supra- and infraduction with possible bradycardia on eye movements. In these presentations, it is recommended that surgical intervention be prompt once entrapment is confirmed.
Fig. 9.6
Coronal (a) and sagittal (b) orbital CT scan showing a large displaced right orbital floor fracture with prolapse of orbital soft tissues into the maxillary sinus
Medial Wall Fracture
The medial wall fracture (Fig. 9.7) most commonly involves the thin ethmoid bone (lamina papyracea). The fracture can be treated conservatively in most cases. The medial rectus muscle can rarely get entrapped within the fracture and in that case the patient would need emergent surgical repair. The patient may show limitation of eye movement on abduction and diplopia in lateral gaze. Due to the close proximity of the medial wall to the ethmoid sinus, fractures can cause orbital emphysema which, if severe, can cause a compartment syndrome. Patients with both large medial and floor fractures are at increased risk of developing enophthalmos and should be monitored for this potential finding on serial clinical exams with Hertel exophthalmometry.
Fig. 9.7
Axial orbital CT scan showing fracture of the left medial wall
Orbital Roof Fractures
Fractures of the orbital roof are usually caused by blunt trauma or projectile missile injuries. They are more common in children as they do not have formed pneumatized frontal sinuses to absorb the impact of the trauma. The majority of roof fractures do not require surgical repair. Any patient who presents with a fracture of the roof warrants a neurosurgical consultation, and intracranial injury must be evaluated and ruled out. If repair were warranted, such as in cases of severe intracranial injury or hematoma, the surgical approach would be done in conjunction with a neurosurgeon. Pulsating proptosis may occur as a delayed complication of severe comminuted orbital roof fracture resulting from the transmission of cerebrospinal fluid pulsations through the bony defect.
Orbital Apex Fracture
Orbital apex fractures involve the optic canal and/or the superior and inferior orbital fissures. This type of fracture can cause traumatic optic neuropathy, multiple cranial neuropathies, and long-term visual morbidity.
Lateral Wall Fracture
Lateral wall fractures are rare given the strength of the zygoma and greater wing of sphenoid. A specific type of fracture known as the zygomaticomaxillary complex (ZMC) or tripod fracture involves the lateral wall. It is a constellation of fractures that includes the zygoma in two locations, the inferior orbital rim and the maxillary sinus wall (Fig. 9.8). Severe ZMC fractures can cause globe dystopia, trismus and malar flattening. Large and displaced fractures especially when in conjunction with a symptomatic patient may warrant surgical repair that typically involves open reduction of the fractures with fixation with titanium plates and screws. Displaced zygoma fractures without surgical repair can lead to an antimongoloid slant of the lids if the lateral canthal tendon attachment to the zygoma becomes displaced.
