Symptoms
Pain with eye movement; local tenderness; eyelid edema; binocular diplopia; crepitus (particularly after nose blowing); and numbness of the cheek, upper lip, and/or teeth. Tearing may be a symptom of nasolacrimal duct obstruction or injury seen with medial buttress, Le Fort II, or nasoethmoidal complex fractures, but this is typically a late complaint. Acute tearing is usually due to ocular irritation (e.g., chemosis, corneal abrasion, iritis).
Signs
Critical
Restricted eye movement (especially in upward gaze, lateral gaze, or both), subcutaneous or conjunctival emphysema, hypesthesia in the distribution of the infraorbital nerve (ipsilateral cheek and upper lip), point tenderness, enophthalmos (may initially be masked by orbital edema and hemorrhage), and hypoglobus.
Other
Epistaxis, eyelid edema, and ecchymosis. Superior rim and orbital roof fractures may manifest hypesthesia in the distribution of the supratrochlear or supraorbital nerve (ipsilateral forehead), ptosis, and step-off deformity along the anterior table of the frontal sinuses (superior orbital rim and glabella). Trismus, malar flattening, and a palpable step-off deformity of the inferior orbital rim are characteristic of tripod (zygomatic complex) fractures. Optic neuropathy may be present secondary to posterior indirect traumatic optic neuropathy (PI-TON) or from a direct mechanism (orbital compartment syndrome [OCS] secondary to retrobulbar hemorrhage, foreign body, etc.; see below).
Differential Diagnosis of Muscle Entrapment in Orbital Fracture
Workup
3-9.3 Coronal and sagittal cuts of a white-eyed blowout fracture (WEBOF) in a patient with an entrapped inferior rectus.
White arrow, entrapped orbital soft tissue; red arrows, orbital floor fracture.
NOTE: |
It is of paramount importance to rule out intraocular and optic nerve injury as quickly as possible in ALL patients presenting with suspected orbital fracture. |
NOTE: |
Pediatric patients are particularly at risk for a unique type of blowout injury: the trapdoor fracture. Because pediatric bones lack complete calcification, they tend to greenstick rather than completely fracture. This results in an initial fracture, herniation of orbital soft tissue (including EOM) through the fracture site, and rapid snapping back of the malleable bone akin to a trapdoor on a spring. Because of the tight reapposition of the fracture edges, the soft tissue trapped within the fracture becomes ischemic. Children with this type of fracture often have a remarkably benign external periocular appearance but significant EOM restriction (usually vertical) on examination; this constellation of findings has been dubbed the white-eyed blowout fracture (WEBOF). Children may present with a vague history, allow only a limited ocular examination, and be misdiagnosed as having an intracranial injury (e.g., concussion) leading to delay in management of WEBOF. Be aware of the oculocardiac reflex (nausea or vomiting, bradycardia, syncope, dehydration) that can accompany entrapment. Even in cases where correct orbital imaging is performed, CT evidence of an orbital fracture may be minimal and routinely missed. Careful examination of coronal and parasagittal views is critical in such cases. In typical (i.e., non-WEBOF) orbital fractures, forced duction testing or testing of the dolls eye reflex may be performed if limitation of eye movement persists beyond 1 week and restriction is suspected. In the early phase, it is often difficult to distinguish soft tissue edema or contusion from soft tissue entrapment in the fracture. SEE APPENDIX 6, FORCED DUCTION TEST AND ACTIVE FORCE GENERATION TEST. |
NOTE: |
In the absence of visual symptoms (subjective change in vision, diplopia, periocular pain, photophobia, floaters or flashes), patients with orbital fractures are unlikely to have an ophthalmic condition requiring intervention within 24 hours. However, all patients with orbital fractures should undergo a complete ophthalmic examination within 48 hours of injury. Any patient complaining of blurred vision, severe pain, or other significant visual symptoms should undergo more urgent ophthalmic evaluation. |
Treatment
NOTE: |
Orbital fracture repair should be deferred or delayed if there is any evidence of full-thickness globe injury or penetrating trauma. Presence of hyphema or microhyphema typically delays orbital fracture repair for 10 to 14 days. |
Immediate Repair (Within 24 to 48 hours)
If there is clinical evidence of muscle entrapment with nonresolving bradycardia, heart block, nausea, vomiting, or syncope (most often encountered in children with WEBOF). Patients with muscle entrapment require urgent orbital exploration to release any incarcerated muscle to decrease the chance of permanent restrictive strabismus from muscle ischemia and fibrosis, as well as to alleviate systemic symptoms from the oculocardiac reflex.
Repair in 1 to 2 Weeks
Delayed Repair
NOTE: |
The role of anticoagulation in postoperative or posttrauma patients is debatable. Anecdotal reports have described orbital hemorrhage in patients with orbital and midfacial fractures who were anticoagulated for prophylaxis against deep vein thrombosis (DVT). On the other hand, multiple large studies have also demonstrated an increased risk of DVT and pulmonary embolism (PE) in postoperative patients who are obtunded or cannot ambulate. At the very least, all inpatients with orbital fractures awaiting surgery and all postoperative orbital fracture patients should be placed on intermittent pneumatic compression (IPC) therapy and encouraged to ambulate. In patients at high risk for DVT, including those who are obtunded from concomitant intracranial injury, a detailed discussion with the primary care team regarding anticoagulation should be documented, and the risks for and against such therapy should be discussed in detail with the patient and family. |
Follow Up
Patients should be seen at 1 and 2 weeks after trauma to be evaluated for persistent diplopia and/or enophthalmos after the acute orbital edema has resolved. If sinusitis symptoms develop or were present prior to the injury, the patient should be seen within a few days of the injury. Patients should also be monitored for development of associated ocular injuries as indicated (e.g., orbital cellulitis, angle-recession glaucoma, retinal detachment). Gonioscopy and dilated fundus examination with scleral depression is performed about 4 weeks after trauma if a hyphema or microhyphema was present. Warning symptoms of retinal detachment and orbital cellulitis are explained to the patient.