Ophthalmology – Fracture, White-Eyed Blowout

Basics

Description

A white-eyed blowout fracture (WEBOF) is a trapdoor or greenstick fracture of the orbital floor or, less commonly, the medial orbital wall that causes entrapment of orbital soft tissue or an extraocular muscle. The entrapped muscle may become ischemic, producing severe restriction of ocular movement and persistent diplopia.

The condition occurs predominantly in children and adolescents, although young adults in their early 20s may also be affected.

The term white-eyed refers to the striking absence of external signs despite a potentially serious orbital injury. There may be little or no eyelid swelling, ecchymosis, or subconjunctival hemorrhage. Consequently, the injury may initially be mistaken for a concussion or minor facial trauma.

White-eyed blowout fracture is also known as a trapdoor orbital fracture.

Epidemiology

White-eyed blowout fractures occur primarily in children and young adults. There is no established racial predilection.

No definite sex predilection has been demonstrated, although males experience traumatic injuries more frequently overall.

The orbital floor is affected more commonly than the medial orbital wall or lamina papyracea.

The exact incidence and prevalence are unknown.

Risk Factors

The major risk factors are young age and recent blunt periocular trauma.

Common mechanisms include sports-related injuries, motor vehicle accidents, falls, and physical altercations.

Prevention

Prevention centers on reducing the risk of orbital trauma.

Children participating in sports should use appropriate polycarbonate protective glasses, goggles, face shields, or other sport-specific eye protection.

Age-appropriate seat belts, car seats, and other restraint systems should be used consistently in motor vehicles.

Pathophysiology

Two principal mechanisms have been proposed for orbital blowout fractures.

In the hydraulic mechanism, a blunt object strikes the globe and orbital entrance, suddenly increasing intraorbital pressure. This pressure is transmitted to the thin orbital floor or medial wall, causing the bone to fracture into an adjacent paranasal sinus.

In the buckling mechanism, a blow to the inferior orbital rim transmits force posteriorly through the orbital skeleton, causing the orbital floor to buckle and fracture.

The Pediatric Trapdoor Mechanism

The orbital bones of children are relatively thin, elastic, and incompletely calcified compared with those of adults.

Following blunt trauma, the orbital floor or medial wall may temporarily bend or crack open. Increased orbital pressure forces orbital fat, connective tissue, and sometimes an extraocular muscle through the opening.

Because pediatric bone is highly elastic, the fractured segment may immediately spring back toward its original position. This creates a trapdoor effect, tightly incarcerating the prolapsed orbital tissue.

The inferior rectus or its surrounding tissues are most commonly involved in orbital floor fractures. The medial rectus or adjacent tissues may be involved with medial wall fractures.

Prolonged incarceration can impair blood flow to the muscle and lead to ischemia, fibrosis, and permanent restrictive strabismus.

Oculocardiac Reflex

One of the most important features of a white-eyed blowout fracture is the oculocardiac reflex.

Traction on or entrapment of an extraocular muscle stimulates trigeminal afferent pathways and produces a vagal response.

Affected patients may develop nausea, vomiting, dizziness, bradycardia, hypotension, syncope, or, rarely, cardiac conduction abnormalities.

The nausea and vomiting can be dramatic and may be mistaken for manifestations of a concussion.

The combination of recent orbital trauma, restricted ocular motility, pain with eye movement, nausea, vomiting, or bradycardia should therefore raise immediate concern for a trapdoor fracture with tissue entrapment.

Etiology

The condition results from blunt periocular trauma.

Sports injuries are particularly common in children, but motor vehicle accidents, falls, and interpersonal trauma can also produce the injury.

Commonly Associated Conditions

Associated ocular injuries may include hyphema, vitreous hemorrhage, choroidal rupture, retinal injury, and other intraocular trauma.

The oculocardiac reflex may produce clinically important bradycardia and, rarely, heart block.

Significant intracranial injury is not a defining feature of white-eyed blowout fracture. Nevertheless, the mechanism of trauma should determine whether concurrent neurologic injury requires investigation.

Diagnosis

History

A typical patient has sustained recent blunt trauma to the periocular region.

The patient may complain of diplopia and significant pain when attempting to move the affected eye.

Nausea and vomiting, particularly when precipitated or worsened by attempted eye movement, are important diagnostic clues.

The absence of dramatic bruising or swelling should not reassure the clinician.

Loss of consciousness is not characteristic of an isolated white-eyed blowout fracture, although associated head injury must still be considered according to the mechanism and clinical findings.

Physical Examination

External Examination

The external appearance may be surprisingly normal.

There may be only minimal eyelid edema, minimal ecchymosis, or a small subconjunctival hemorrhage despite significant tissue entrapment.

This discrepancy between a relatively quiet external appearance and severe functional impairment is the hallmark of the condition.

Ocular Motility

Marked restriction of ocular movement is a major finding.

With an orbital floor trapdoor fracture, vertical motility is usually impaired, particularly upgaze, although the exact pattern depends on which tissues are incarcerated.

With a medial wall trapdoor fracture, horizontal motility may be restricted.

The child may refuse to open or move the eye because attempted movement produces significant pain, nausea, or vomiting.

Diplopia

Diplopia results from mechanical restriction of the entrapped muscle or surrounding connective tissues.

The severity of diplopia does not necessarily correlate with the amount of external swelling.

Facial Sensation

Contusion or injury of the infraorbital nerve may produce numbness or altered sensation over the cheek, upper lip, or lateral nose when the orbital floor is involved.

Complete Ophthalmic Examination

A complete examination is essential to exclude associated globe, retinal, and optic nerve injuries.

Visual acuity, pupillary responses, ocular motility, anterior segment findings, intraocular pressure when appropriate, and the posterior segment should be assessed.

Diagnostic Tests and Interpretation

CT Imaging

Thin-section CT of the orbits with multiplanar reconstruction is the preferred imaging study.

Both bone and soft-tissue windows should be reviewed carefully.

White-eyed blowout fractures can be subtle and easily missed on CT because the elastic fractured bone may return nearly to its normal position after trapping the orbital tissues.

Consequently, a CT report describing little or no displacement does not exclude clinically important entrapment when the history and examination are strongly suggestive.

Dedicated orbital imaging is preferable because a routine head CT may not provide sufficiently detailed evaluation of the orbital walls and extraocular muscles.

In children, radiation exposure should be minimized using appropriate pediatric CT protocols.

MRI and Plain Radiographs

Plain radiographs provide inadequate detail and are generally not useful when modern CT imaging is available.

MRI is not the initial study of choice for acute orbital fractures because CT provides superior assessment of the bony orbital anatomy.

Intracranial Imaging

Additional evaluation for intracranial trauma should be performed when indicated by the mechanism of injury, neurologic examination, or other concerning symptoms.

Other Diagnostic Considerations

If the patient has significant persistent bradycardia or another manifestation of the oculocardiac reflex, cardiac monitoring may be necessary.

In severe cases, hospital admission may be appropriate while definitive treatment is arranged.

Pathologically, the fracture may trap the extraocular muscle itself or only the perimuscular fascia, connective tissue, and orbital fat. Either situation can produce substantial restriction of ocular movement.

Differential Diagnosis

Concussion or Intracranial Injury

Nausea and vomiting following trauma can lead to an incorrect diagnosis of concussion.

The presence of marked ocular motility restriction and symptoms provoked by eye movement should raise suspicion for a trapdoor fracture and oculocardiac reflex.

Extraocular Muscle Contusion

Orbital trauma without entrapment can cause muscle edema and contusion, resulting in temporary diplopia and motility limitation.

However, simple contusion generally does not produce the pronounced oculocardiac symptoms associated with significant trapdoor entrapment.

Treatment

White-eyed blowout fracture with clinically significant entrapment is considered an urgent surgical condition.

Medical therapy alone cannot release incarcerated tissue.

The objective is to free the entrapped tissue before prolonged ischemia and fibrosis result in permanent restrictive strabismus.

Timing of Surgery

Patients with convincing clinical evidence of extraocular muscle or soft-tissue entrapment should receive urgent orbital surgical evaluation and prompt repair.

Surgery should not be unnecessarily delayed solely to allow orbital swelling to resolve, as might be appropriate for some uncomplicated adult blowout fractures.

Marked motility restriction associated with pain, nausea, vomiting, bradycardia, or other manifestations of the oculocardiac reflex strengthens the indication for urgent intervention.

Earlier literature commonly advocated repair within approximately 24–72 hours. In practice, the urgency is determined by the severity of entrapment and systemic manifestations, with significant oculocardiac reflex or severe restriction generally warranting particularly rapid intervention.

Preoperative Management

The patient should remain NPO when urgent surgery is anticipated.

Severe vomiting may result in dehydration, particularly when symptoms have persisted for many hours or days. Intravenous fluid replacement may therefore be necessary.

Antiemetics can be administered for symptomatic relief, although they may not fully control symptoms while the tissue remains entrapped.

The patient should undergo a complete ophthalmic examination and appropriate orbital imaging before surgery whenever the clinical situation permits.

Cardiac monitoring should be considered when significant bradycardia or conduction abnormalities are present.

Antibiotics and Corticosteroids

Some clinicians prescribe short courses of systemic antibiotics after orbital fracture repair, particularly when there is concern about sinus contamination. However, routine prophylactic antibiotics in otherwise uncomplicated closed fractures have limited supporting evidence.

Systemic corticosteroids have also historically been prescribed in an attempt to reduce post-traumatic edema and fibrosis. Their routine benefit in white-eyed blowout fractures has not been firmly established.

Neither antibiotics nor corticosteroids should delay definitive release of entrapped tissue.

Surgery and Other Procedures

Surgical treatment consists of orbital exploration and release of the incarcerated muscle, fascia, fat, and other soft tissues.

After the tissue is released, the surgeon assesses the residual orbital wall defect.

If the trapdoor bone returns to an appropriate position and there is no risk of recurrent entrapment, an implant may not always be necessary.

More commonly, a residual defect remains after tissue release. An orbital implant may then be positioned across the defect to prevent recurrent herniation or re-entrapment.

Both absorbable and nonabsorbable materials may be used according to the clinical situation and surgeon preference.

Many orbital floor trapdoor fractures can be repaired through a transconjunctival approach, avoiding an external skin incision.

Inpatient Considerations

Admission

Hospital admission may be required for intractable nausea and vomiting, dehydration, clinically important bradycardia, cardiac conduction abnormalities, or other associated injuries.

Postoperative Monitoring

Following successful release of entrapped tissue, nausea and vomiting caused by the oculocardiac reflex usually improve rapidly.

Visual acuity, pupils, pain, and orbital swelling should be monitored after surgery because postoperative orbital hemorrhage can rarely cause orbital compartment syndrome and compressive optic neuropathy.

Unexpected severe pain, rapidly increasing proptosis or swelling, reduced vision, or a new pupillary abnormality requires immediate assessment.

Cold compresses can be used during the early postoperative period to reduce edema and discomfort.

Postoperative Diplopia

Persistent diplopia immediately after successful surgery is common and does not necessarily indicate surgical failure.

The entrapped muscle may have sustained edema, ischemia, contusion, or neuropraxia. Ocular motility can therefore take weeks to months to recover.

Patients and their families should be counseled about this possibility before surgery.

In contrast, persistent or recurrent nausea, vomiting, severe movement-related pain, or other oculocardiac symptoms after repair may raise concern for inadequate release or recurrent entrapment and should prompt reassessment.

Ongoing Care and Follow-Up

Patients are usually reviewed within approximately one week after repair, with subsequent follow-up based on ocular motility and recovery.

Cold compresses are generally continued during the first few postoperative days.

Patients should avoid nose blowing, strenuous exercise, heavy lifting, and contact sports during the initial healing period as directed by the treating surgeon.

Visual function should be monitored carefully, and patients and families should be educated about symptoms of postoperative orbital hemorrhage.

A repeat dilated retinal examination may be appropriate after the acute injury period to identify delayed manifestations of associated ocular trauma.

Management of Persistent Diplopia

Temporary occlusion of one eye may be used for troublesome postoperative diplopia.

Care must be taken in young children because prolonged monocular occlusion can cause or worsen amblyopia.

Persistent ocular misalignment should be followed with serial measurements while the injured muscle recovers.

Definitive strabismus surgery should generally be deferred until ocular alignment and motility have stabilized, often for several months, because substantial spontaneous improvement may occur following timely fracture repair.

Patient Monitoring

The most important parameters during follow-up are visual acuity, pupillary function, ocular alignment, extraocular motility, diplopia, globe position, and recovery of facial sensation.

Persistent motility restriction does not necessarily indicate a poor outcome early after surgery. Improvement may continue gradually over weeks or months.

Prognosis

The prognosis is generally excellent when significant entrapment is recognized and released promptly.

Most appropriately treated patients experience substantial recovery of extraocular motility and resolution of diplopia in functionally important positions of gaze.

Some residual diplopia may remain in extreme gaze, particularly upgaze, without causing significant functional disability.

Delayed recognition and prolonged incarceration increase the risk of muscle ischemia, fibrosis, restrictive strabismus, and persistent diplopia.

Complications

One of the most important complications is delayed or missed diagnosis, particularly when the injury is mistaken for concussion or when a subtle fracture is overlooked on imaging.

Persistent diplopia and restrictive strabismus may occur because of ischemic or fibrotic damage to the entrapped muscle.

Surgical complications include orbital hemorrhage, compressive optic neuropathy, persistent infraorbital sensory disturbance, eyelid malposition, scarring, implant migration or extrusion, sinusitis, and orbital cellulitis.

Enophthalmos and hypoglobus are possible but are generally less prominent than in large adult blowout fractures because pediatric trapdoor fractures often involve relatively small bony defects.

The key clinical principle is that a child with minimal external trauma but severe ocular motility restriction, pain with eye movement, nausea, vomiting, or bradycardia should be presumed to have significant orbital entrapment until appropriately evaluated.