Ophthalmology – Fractures, Orbital Medial Wall

Basics

Description

An orbital medial wall fracture is a traumatic defect involving the bony medial wall of the orbit. The medial wall is formed mainly by the ethmoid bone, with contributions from the lacrimal, maxillary, and sphenoid bones.

Medial wall fractures may occur as extensions of other facial fractures or together with an orbital floor fracture. An isolated indirect or blowout fracture of the medial wall can also occur without disruption of the orbital rim.

Because the medial orbital wall is very thin, trauma may permit orbital fat and occasionally the medial rectus muscle or adjacent soft tissues to herniate into the ethmoid sinuses. This can lead to diplopia, ocular motility restriction, enophthalmos, or globe dystopia.

Epidemiology

The incidence and prevalence of medial orbital wall fractures vary according to the population and mechanism of injury. They are frequently seen in association with broader orbital or midfacial trauma.

Risk Factors

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

Important risk factors include participation in contact or projectile sports and activities associated with facial trauma. Substance use may indirectly increase risk through falls, interpersonal violence, and motor vehicle accidents.

Prevention

Protective eyewear should be used during sports and occupational activities involving high-velocity objects.

Sports such as baseball, softball, and hockey are important examples in which appropriate eye and facial protection can reduce the risk of orbital trauma.

Pathophysiology

Medial wall blowout fractures frequently occur together with orbital floor blowout fractures, although isolated medial wall fractures can also occur.

Blunt trauma to the orbital entrance can cause a sudden increase in intraorbital pressure. Because the medial wall is extremely thin, especially at the lamina papyracea, it may fracture under this pressure.

Orbital fat may then herniate into the ethmoid sinus. In more severe cases, the medial rectus muscle or surrounding connective tissue can become trapped within the fracture.

Entrapment may produce restricted horizontal ocular movement and diplopia. Large defects can also increase orbital volume and later result in enophthalmos or abnormal globe position.

Etiology

The main cause is blunt orbital or facial trauma.

A classic mechanism involves the orbital entrance being struck by an object larger than the diameter of the orbital opening, such as a fist, ball, dashboard, or other blunt object.

Commonly Associated Conditions

Medial orbital wall fractures may coexist with significant ocular injuries, including globe rupture, hyphema or microhyphema, traumatic iritis, commotio retinae, choroidal rupture, and traumatic optic neuropathy.

Because these associated conditions can threaten vision independently of the fracture itself, a complete ocular examination is essential.

Diagnosis

History

A careful history should establish the timing, mechanism, direction, and severity of the trauma.

Patients should be asked about decreased vision, diplopia, ocular pain, facial numbness, and changes in globe position.

A history of nausea, vomiting, or bradycardia, especially when triggered by eye movement, raises concern for extraocular muscle or soft-tissue entrapment causing an oculocardiac reflex.

This is particularly important in children and in patients with an associated orbital floor fracture.

Physical Examination

Periorbital Findings

Patients may develop eyelid edema and ecchymosis following the injury.

Because the medial orbital wall communicates with the ethmoid sinuses, air may enter the orbital and eyelid tissues, producing orbital or eyelid emphysema. Subcutaneous crepitus may sometimes be detected on examination.

Visual Assessment

Visual acuity should be documented in both eyes whenever possible.

Pupillary examination is essential because a relative afferent pupillary defect may indicate significant retinal or optic nerve injury.

A complete anterior and posterior segment examination should be performed to identify associated traumatic ocular pathology.

Diplopia and Ocular Motility

Patients may develop diplopia due to orbital edema, hemorrhage, muscle contusion, or mechanical entrapment.

Entrapment of the medial rectus muscle or adjacent tissues can produce horizontal motility restriction.

Ocular movements should therefore be carefully assessed in all directions of gaze.

Globe Dystopia

Large medial wall fractures may allow orbital contents to herniate into the ethmoid sinus.

This increases effective orbital volume and can lead to enophthalmos or other globe displacement. Enophthalmos may initially be masked by acute swelling and become more apparent after edema resolves.

Forced-Duction Testing

Forced-duction testing can be useful when it is necessary to distinguish mechanical restriction from a neurogenic ocular motility disorder.

Resistance to passive movement supports a restrictive process, whereas normal passive movement is more consistent with a paralytic cause.

This test is not necessary in every patient and should be performed only when clinically appropriate.

Diagnostic Tests and Interpretation

Imaging

CT of the orbits with thin sections and multiplanar reconstruction is the principal imaging study for suspected medial orbital wall fractures.

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

Imaging findings should always be correlated with the clinical examination because herniation seen on CT does not necessarily mean that clinically significant entrapment is present.

Differential Diagnosis

Orbital hemorrhage or edema without fracture can produce swelling, diplopia, and motility limitation, but CT demonstrates no corresponding bony defect.

A cranial nerve palsy can also produce ocular misalignment and diplopia. Unlike mechanical entrapment, forced-duction testing is generally normal.

Other possibilities include extraocular muscle contusion, orbital hematoma, traumatic neuropathy, and associated orbital floor fractures.

Treatment

Management depends on the size of the fracture, presence of soft-tissue or muscle entrapment, diplopia, ocular motility, globe position, associated ocular injuries, and the age of the patient.

Many uncomplicated medial wall fractures can be managed conservatively.

Initial Management

The immediate priority is to identify and treat any associated vision-threatening ocular or orbital injury.

Cold compresses can be used during the early period after trauma to reduce swelling.

Patients should be instructed to avoid nose blowing, because increased sinus pressure can force additional air or contaminated sinus contents into the orbit.

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

Antibiotics

Older protocols often recommended prophylactic broad-spectrum oral antibiotics because the fracture communicates with the paranasal sinuses.

In current practice, routine prophylactic antibiotics for every uncomplicated closed orbital fracture are not universally required.

Antibiotics may be appropriate when there are additional risk factors such as active sinusitis, contaminated wounds, open fractures, immunocompromise, or other significant infectious risks.

Corticosteroids

A short course of systemic corticosteroids may occasionally be considered when there is substantial orbital edema.

Their main purpose is to reduce swelling and facilitate assessment of ocular motility. They are not routinely required for every fracture.

Referral

Patients with orbital trauma should receive appropriate ophthalmologic assessment to exclude associated ocular injuries.

Patients with significant diplopia, persistent motility restriction, enophthalmos, a large fracture, or suspected tissue entrapment should be referred to an oculoplastic or orbital surgeon or another surgeon experienced in orbital fracture management.

Urgent Referral

Patients with nausea, vomiting, or bradycardia associated with restricted ocular movement require urgent specialist evaluation because these findings may indicate extraocular muscle entrapment with an oculocardiac reflex.

Such patients may require urgent surgical release.

Pediatric Considerations

Children may develop a characteristic trapdoor fracture.

Because pediatric orbital bones are relatively elastic, a fractured segment can temporarily displace and then recoil toward its original position, trapping orbital soft tissue or an extraocular muscle.

This can produce a white-eyed blowout fracture, in which severe motility restriction and systemic symptoms occur despite minimal external bruising.

A child with orbital trauma and diplopia, marked motility restriction, nausea, vomiting, or bradycardia should be considered to have possible entrapment even if the external examination appears relatively normal.

When entrapment is confirmed or strongly suspected, early surgical release is generally indicated.

Surgery and Other Procedures

Not all medial wall fractures require surgery.

Surgical repair may be considered when there is persistent functionally significant diplopia with mechanical restriction, clinically important enophthalmos or globe dystopia, significant soft-tissue entrapment, or a large defect likely to cause late orbital volume expansion.

A medial wall fracture that is continuous with a large orbital floor fracture may be more likely to require reconstruction.

Historically, enophthalmos greater than approximately 2 mm has been used as one factor supporting surgical repair when cosmetically or functionally significant.

For nonurgent fractures requiring reconstruction, surgery is commonly performed after acute swelling improves, often within approximately 1–2 weeks, although timing should be individualized.

Entrapment associated with an oculocardiac reflex, particularly in children, may require much earlier surgery.

Surgical Approaches

An orbital floor approach through an eyelid or transconjunctival incision can be extended superiorly to expose the medial wall when both areas require repair.

An isolated medial wall fracture can also be approached through a transcaruncular incision, which provides direct access to the medial orbit without an external skin incision.

During surgery, entrapped tissue is released and the defect may be reconstructed with an orbital implant when necessary to restore orbital volume and prevent recurrent herniation.

Ongoing Care and Follow-Up

Follow-up should assess visual acuity, pupillary responses, ocular motility, diplopia, globe position, and resolution of swelling and orbital emphysema.

Patients may require continued care from an ophthalmologist, with involvement of oculoplastic surgery, otolaryngology, or oral and maxillofacial surgery depending on the associated injuries.

Persistent or worsening diplopia, progressive enophthalmos, new visual loss, increasing pain, fever, proptosis, or worsening motility restriction requires reassessment.

Patient Education

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

They should seek urgent medical attention for new or worsening vision loss, severe ocular pain, increasing redness or swelling, fever, worsening diplopia, or nausea and vomiting associated with eye movement.

Prognosis

The prognosis depends primarily on the severity of the initial trauma and associated ocular, orbital, and facial injuries.

Many uncomplicated medial wall fractures heal well with conservative management.

Patients with significant extraocular muscle entrapment, extensive tissue herniation, traumatic optic neuropathy, or major associated globe injury have a more guarded prognosis.

Complications

Potential complications include decreased vision, persistent diplopia, restrictive strabismus, enophthalmos, and abnormal globe position.

Entrapped extraocular muscle or soft tissue can result in persistent motility dysfunction if not recognized and managed appropriately.

Because the medial wall communicates with the ethmoid sinuses, infection can occasionally spread into the orbit and produce orbital cellulitis.

The most serious visual complications generally result from associated injuries such as globe rupture, retinal damage, or traumatic optic neuropathy, rather than from the medial wall fracture itself.