Orbital Trauma
Joshua Gentges
Douglas Marx
THE CLINICAL CHALLENGE
The orbit is defined by the bony structures that form the orbital floor and wall. It contains and protects many important soft tissue structures, including the eye, extraocular muscles, blood vessels, fascia, ligaments, and cranial nerves (CN) to the orbital structures and face.1 It also contains the eyelids, tear glands, and lacrimal glands (Figure 28.1). Because of the complex bony and soft tissue anatomy, trauma can lead to significant intraocular and extraocular pathology. Careful attention to a focused history and physical examination is important, because missed orbital trauma may lead to loss of vision, intracranial infection, or death in the setting of penetrating orbital injuries.2
The diagnosis of orbital injuries is not always apparent because trauma patients may have distracting injuries, have altered mental status, or be unable to participate in a complete examination. Injuries to the orbit can cause orbital fractures, which can lead to organ threatening pathology, including orbital compartment syndrome (OCS), entrapment of extraocular muscles and other intraorbital tissue, globe rupture, vascular injury, optic neuropathy, or nerve avulsion. Evaluation for entrapment of orbital contents is particularly challenging in trauma patients. External signs of injury may not be present in all cases. OCS is clinically challenging because it is both rare (0.088% of craniomaxillofacial [CMF] injuries) and devastating, leading to vision loss that is progressive with increased time to intervention.2,3,4
PATHOPHYSIOLOGY
Assaults cause most orbital fractures (˜40%), followed by falls (˜25%), recreational or sports related injuries (˜16%), and motor vehicle incidents (˜13%).2 The mechanism for orbital fractures can be either direct trauma to the bone or increased intraorbital pressure, causing a “blowout” fracture.5 Orbital fractures account for half of all facial fractures, and nearly half of these (47.9%) involve the orbital floor, which can lead to entrapment of intraocular tissues, extraocular musculature, or orbital infection.2 More extensive fractures can lead to loss of support of the eye, causing inferior displacement of the eye (hypophthalmos) and diplopia.6
The medial orbital wall is the thinnest part of the orbit, but fractures less commonly owing to reinforcement by the ethmoid. Medial orbital wall fractures can lead to orbital emphysema, tear outflow obstruction, injury to the ethmoidal arteries, and medial rectus entrapment.6 Lateral wall fractures are also less common because of the relative thickness of the lateral wall and its association with the zygomatic bone and the orbital rim. A lateral wall fracture is usually caused by direct force to the cheek and fracture to the zygomatic arch. Orbital roof fractures occur in the setting of high-impact injuries to the head and face. An orbital roof fracture is usually associated with additional facial fractures and neurologic injury.2
An orbital fracture can cause entrapment of intraocular fat, extraocular musculature, or direct damage to the globe. Intraocular fat can herniate through a medial or inferior wall fracture, causing pain with extraocular muscle movement and inflammation. Extraocular muscles can also herniate through an orbital fracture. If the fractured bone “rebounds” from the fracture faster than the muscle, the muscle will become entrapped in the fracture, causing reduced ocular motility and
diplopia. This is more common in children and young adults because the bone in these populations is more elastic.7 Clinicians should be aware of the oculocardiac reflex, vagally mediated bradycardia with nausea, vomiting, and vertigo caused by extraocular muscle entrapment most commonly in the orbital floor. This finding in isolated facial trauma should prompt rapid evaluation for orbital fracture with entrapment and increase the urgency of primary repair of a facial fracture.8,9
diplopia. This is more common in children and young adults because the bone in these populations is more elastic.7 Clinicians should be aware of the oculocardiac reflex, vagally mediated bradycardia with nausea, vomiting, and vertigo caused by extraocular muscle entrapment most commonly in the orbital floor. This finding in isolated facial trauma should prompt rapid evaluation for orbital fracture with entrapment and increase the urgency of primary repair of a facial fracture.8,9
 Figure 28.1: Orbital Cavity and Surface Anatomy of Eye A. Bones and features of orbital cavity. B. and C. Surface anatomy of eye. (From Agur AMR, Dalley AF II. Grant’s Atlas of Anatomy. 15th ed. Wolters Kluwer; 2021. Figure 7.36.) |
Orbital fractures, or even an orbital contusion without fracture, can lead to increased intraorbital pressure from orbital emphysema, hemorrhage, inflammatory changes, or infection when presentation is delayed. Increasing pressures can lead to OCS with multiple downstream effects, including ischemia; damage to the optic nerve and retina; and rapid, progressive vision loss.3 As intraorbital pressure increases, the orbital contents move toward the area of least resistance, in most cases the front of the orbit, causing exophthalmos.
Direct trauma to intraorbital components can result in globe penetration or rupture, which are ophthalmologic emergencies. Optic nerve transection or neuropathy, hyphema, foreign body, traumatic cataract, and retinal detachment can also occur. In general, these injuries require urgent but not necessarily emergent ophthalmologic referral and intervention.2 Intraorbital trauma often
occurs concomitantly with orbital fractures,7 so emergency clinicians must maintain a high level of suspicion for intraorbital injury when diagnosing an orbital fracture.
occurs concomitantly with orbital fractures,7 so emergency clinicians must maintain a high level of suspicion for intraorbital injury when diagnosing an orbital fracture.
