Ophthalmology – Orbital Floor Fractures

Basics

Description

An orbital floor fracture is a traumatic disruption of the bony floor of the orbit. The fracture may occur as an extension of an inferior orbital rim fracture, or it may occur as an isolated blowout fracture.

An indirect or blowout fracture occurs when the orbital floor fractures while the orbital rim remains intact. Orbital soft tissues, including orbital fat and occasionally an extraocular muscle, may herniate or become entrapped within the fracture defect. This can produce diplopia, restricted ocular motility, enophthalmos, and infraorbital sensory loss.

Epidemiology

The incidence and prevalence of orbital floor fractures vary according to population and mechanism of injury. They are particularly common following facial trauma in adolescents and young adults.

Risk Factors

Orbital floor fractures occur more commonly in males and younger individuals, particularly those between approximately 15 and 30 years of age.

Participation in contact or projectile sports increases the risk. Substance use may also increase risk through its association with interpersonal violence, falls, and motor vehicle trauma.

Prevention

Appropriate protective eyewear should be worn during sports and occupations involving high-velocity objects.

Sports such as baseball, softball, and hockey are important examples in which properly fitted protective equipment can reduce the risk of orbital and ocular trauma.

Pathophysiology

Two principal mechanisms have traditionally been proposed to explain orbital floor blowout fractures.

The hydraulic theory proposes that a relatively large, nonpenetrating object strikes the orbital entrance and rapidly increases intraorbital pressure. The globe and orbital contents are displaced posteriorly, transmitting pressure to the orbital walls. The weakest portion of the orbit then fractures, commonly involving the thin posterior-medial orbital floor overlying the maxillary sinus.

The buckling theory proposes that an impact to the inferior orbital rim transmits a compressive force posteriorly through the orbital bones. This causes the relatively thin orbital floor to buckle and fracture even when the orbital rim itself remains intact.

Following either mechanism, orbital fat and other soft tissues may prolapse into the maxillary sinus. In some patients, the inferior rectus muscle or surrounding connective tissue becomes entrapped, producing restrictive ocular motility.

Etiology

Orbital floor fractures are caused by blunt facial or orbital trauma.

A classic mechanism involves an object larger than the orbital opening, such as a fist, ball, dashboard, or other blunt object, striking the orbital region.

Associated Ocular Injuries

Because considerable force may be required to produce an orbital fracture, a complete evaluation for associated ocular trauma is essential.

Potential associated injuries include globe rupture, hyphema or microhyphema, traumatic iritis, commotio retinae, choroidal rupture, and traumatic optic neuropathy.

These injuries may be more immediately vision-threatening than the orbital fracture itself.

Diagnosis

History

The clinician should determine the exact mechanism, timing, and severity of trauma.

Patients should be questioned about diplopia, decreased vision, ocular pain, facial numbness, and changes in the position of the eye.

A classic history involves blunt trauma from an object larger than the orbital opening.

Particular attention should be given to nausea, vomiting, dizziness, or bradycardia after orbital trauma. These findings can indicate an oculocardiac reflex caused by extraocular muscle or soft-tissue entrapment and may require urgent surgical assessment.

Physical Examination

Examination commonly demonstrates periorbital edema and ecchymosis.

Visual acuity, pupils, intraocular structures, and the posterior segment should be examined carefully to exclude associated ocular injury.

Ocular Motility and Diplopia

Diplopia may occur because of edema, hemorrhage, muscle contusion, nerve injury, or mechanical entrapment.

Patients with orbital floor fractures commonly have limitation of upgaze, downgaze, or both, depending on the tissues involved.

Persistent restriction, particularly when accompanied by nausea, vomiting, or bradycardia, raises concern for entrapment.

Globe Position

Enophthalmos may occur when orbital contents herniate through a sufficiently large floor defect, effectively increasing orbital volume.

The globe may also become displaced inferiorly, producing hypoglobus.

Significant enophthalmos may initially be concealed by acute orbital edema and become more apparent after the swelling subsides.

Infraorbital Sensation

Damage or compression of the infraorbital nerve may cause hypesthesia or paresthesia of the lower eyelid, cheek, lateral nose, and upper lip on the affected side.

Orbital Emphysema

Air may enter the orbit from the adjacent maxillary sinus, producing orbital or eyelid emphysema.

For this reason, patients should be instructed not to blow their nose following an orbital fracture.

Orbital Rim

Palpation may reveal tenderness or a step-off deformity when the fracture extends to involve the orbital rim.

Forced-Duction Testing

Forced-duction testing can help distinguish mechanical restriction from a neurogenic motility deficit.

After appropriate topical anesthesia, the globe is gently manipulated to determine whether passive movement is mechanically restricted.

A positive forced-duction test supports restrictive entrapment. However, the need for this test depends on the clinical situation, and imaging plus specialist examination frequently provides the necessary information.

Diagnostic Testing

Imaging

CT of the orbits with thin sections and multiplanar reconstruction is the principal imaging study for suspected orbital floor fracture.

CT can demonstrate the location and extent of the bony defect, herniation of orbital fat into the maxillary sinus, associated orbital wall fractures, and displacement or possible entrapment of extraocular muscles and adjacent soft tissues.

Importantly, radiographic herniation of tissue does not by itself establish clinically significant entrapment. The CT findings must be interpreted together with ocular motility, symptoms, and the remainder of the clinical examination.

Differential Diagnosis

Orbital hemorrhage and edema without fracture may produce swelling, proptosis, diplopia, and restricted movement, but CT does not demonstrate a bony fracture.

A cranial nerve palsy may also cause diplopia and ocular motility abnormalities. Unlike a mechanically restrictive fracture, passive globe movement is generally not restricted.

Muscle contusion, traumatic neuropathy, orbital hematoma, and other orbital injuries should also be considered.

Treatment

Treatment depends on the size of the fracture, presence of tissue entrapment, ocular motility, diplopia, globe position, associated injuries, and the patient’s age.

Not every orbital floor fracture requires surgery.

Initial Management

The first priority is identification and management of potentially vision-threatening injuries, particularly open-globe injury, orbital compartment syndrome, retinal injury, and traumatic optic neuropathy.

Cold compresses can be used during the early post-traumatic period to reduce swelling.

Patients should be specifically instructed to avoid nose blowing, because increased intranasal pressure may force air or contaminated sinus material through the fracture into the orbit.

Nasal decongestants may be considered in selected patients when not otherwise contraindicated.

Analgesia should be provided as necessary.

Antibiotics

Older treatment protocols frequently recommended prophylactic broad-spectrum oral antibiotics, particularly when an orbital fracture communicated with a paranasal sinus.

In contemporary practice, routine prophylactic antibiotics for every uncomplicated closed orbital floor fracture are not universally recommended, because evidence supporting their benefit is limited.

Antibiotic therapy may nevertheless be appropriate in selected patients, such as those with contaminated wounds, active sinus infection, open fractures, immunocompromise, or other increased infectious risk. Management should therefore be individualized.

Corticosteroids

A short course of systemic corticosteroids may occasionally be considered when substantial orbital edema makes assessment of ocular motility difficult.

They are not mandatory for every orbital floor fracture, and contraindications to systemic corticosteroid therapy must be considered.

Referral

Patients with an orbital floor fracture should receive appropriate ophthalmic assessment to exclude associated ocular injuries.

Patients with persistent diplopia, significant motility restriction, enophthalmos, large fractures, or suspected entrapment should be evaluated by an oculoplastic/orbital surgeon or other surgeon experienced in orbital fracture management.

Routine nonurgent fractures can generally be reassessed after the initial edema begins to resolve.

Urgent Referral

Suspected extraocular muscle or soft-tissue entrapment requires urgent specialist assessment.

The combination of restricted eye movement with nausea, vomiting, or bradycardia is particularly concerning because it may represent the oculocardiac reflex.

This situation should not simply be observed for several days while awaiting resolution of swelling.

Pediatric Considerations

Children can sustain a characteristic trapdoor orbital floor fracture. Because pediatric bone is relatively elastic, the fractured bone may temporarily displace and then recoil toward its original position, trapping extraocular muscle or orbital soft tissue.

External bruising and swelling may be surprisingly mild, producing the so-called white-eyed blowout fracture.

A child with orbital trauma, marked motility restriction, diplopia, nausea, vomiting, or bradycardia should therefore be considered to have possible entrapment even when external signs appear minor.

Confirmed or strongly suspected pediatric entrapment generally requires urgent surgical evaluation and early release of the entrapped tissue.

Surgical Treatment

Many orbital floor fractures can be managed conservatively, particularly when diplopia is improving, ocular motility is recovering, and clinically significant enophthalmos is absent.

Surgery is considered when there is persistent functionally significant diplopia with restrictive motility, clinically important enophthalmos or hypoglobus, a sufficiently large defect likely to produce significant late globe displacement, or confirmed tissue entrapment.

Historically, involvement of approximately 50% or more of the orbital floor has been used as one factor suggesting an increased risk of late enophthalmos. However, fracture size alone should not determine management.

Similarly, enophthalmos greater than approximately 2 mm may support repair when it is clinically or cosmetically significant.

For fractures requiring nonurgent reconstruction, surgery is commonly performed after initial swelling has improved but before fibrosis becomes established, often within approximately 1–2 weeks. The timing should be individualized.

Entrapment associated with an oculocardiac reflex or a pediatric trapdoor fracture may require substantially earlier intervention.

Surgical Procedure

The goals of surgery are to release entrapped orbital tissue, restore orbital anatomy and volume, and support the orbital contents.

Entrapped tissues are carefully freed from the fracture site. An orbital implant or other reconstructive material may then be positioned over the bony defect to separate the orbital contents from the maxillary sinus and restore the contour of the orbital floor.

Follow-Up

Patients should be monitored for changes in visual acuity, pupils, ocular motility, diplopia, globe position, and infraorbital sensation.

Follow-up with ophthalmology is appropriate, with involvement of oculoplastic surgery, otolaryngology, or oral and maxillofacial surgery according to the fracture pattern and local treatment approach.

Persistent or worsening visual loss, increasing pain, proptosis, severe motility restriction, fever, or new neurologic symptoms requires prompt reassessment.

Patient Education

Patients should understand that the fracture itself is only one component of orbital trauma and that associated ocular injuries may determine the ultimate visual outcome.

They should avoid nose blowing and activities that markedly increase sinonasal pressure during the early healing period.

New or worsening vision loss, severe pain, increasing swelling, fever, worsening diplopia, nausea or vomiting associated with eye movement, or other significant changes should prompt urgent medical evaluation.

Prognosis

The prognosis is generally favorable in uncomplicated orbital floor fractures.

Final outcome depends largely on the severity of the initial trauma, associated ocular injuries, degree of soft-tissue damage, presence of entrapment, and development of late enophthalmos or persistent diplopia.

Early recognition of muscle entrapment is particularly important because prolonged ischemia and fibrosis can result in persistent motility dysfunction.

Complications

Important complications include persistent diplopia, restrictive strabismus, enophthalmos, hypoglobus, and persistent infraorbital nerve hypesthesia.

Visual loss may occur because of associated globe, retinal, or optic nerve injury rather than from the floor fracture itself.

Less commonly, infectious complications such as orbital cellulitis may develop, particularly when infection spreads from an adjacent paranasal sinus.