Orbital Trauma: Blow-Out Fractures, Optic Nerve Compression and Emergency Care

Orbital trauma can threaten vision through globe injury, muscle entrapment, retrobulbar haemorrhage, direct optic-nerve compression or traumatic optic neuropathy. It can also coexist with facial, brain, sinus and cervical-spine injuries. The first task is to stabilize life-threatening trauma, identify immediately reversible threats to sight, and avoid pressure on a possible open globe. This teaching post covers the complete supplied 93-slide orbital-trauma deck, including orbital anatomy, midface fractures, blow-out fractures, orbital compartment syndrome, optic-nerve injury and intraorbital foreign bodies.

Learning objectives

• Recall the orbital bones, walls, openings, muscles and neighbouring sinuses that explain common trauma patterns.
• Perform a structured orbital assessment after the trauma primary survey and recognize signs of globe, optic-nerve, muscle, cranial-base and midface injury.
• Explain the mechanism, presentation, imaging and referral pathway for orbital floor blow-out fracture, including paediatric trapdoor entrapment.
• Distinguish orbital compartment syndrome with pressure-related optic-nerve ischaemia from traumatic optic neuropathy caused by direct or indirect nerve injury.
• Recognize orbital roof, medial wall/naso-orbito-ethmoid (NOE), Le Fort and zygomaticomaxillary complex (ZMC) injuries and their associated complications.
• Describe safe emergency management, indications for urgent specialist surgery, and decisions about intraorbital foreign bodies.

1. Orbital anatomy for emergency assessment

The orbit is a cone-shaped bony cavity with an anterior opening and a narrow apex. It contains the globe, extraocular muscles, optic nerve, cranial nerves, ophthalmic vessels, lacrimal structures, orbital fat and connective-tissue septa. Its walls separate the orbit from the cranial cavity, nasal cavity and paranasal sinuses. A seemingly local orbital injury can therefore involve the brain, skull base, airway, facial skeleton, globe, optic nerve or sinuses.

The optic canal transmits the optic nerve and ophthalmic artery. The superior orbital fissure transmits cranial nerves III, IV, V1 and VI plus sympathetic fibres and veins. The inferior orbital fissure communicates with the pterygopalatine and infratemporal fossae and transmits branches including infraorbital nerve and vessels. The infraorbital nerve travels in the floor before emerging on the cheek; numbness of the lower eyelid, cheek, upper lip, upper teeth or gingiva suggests V2 involvement. The supraorbital nerve is a V1 branch; forehead/scalp numbness may accompany roof/rim injury.

Orbital floor lies above the maxillary sinus; the medial wall borders ethmoid sinus. These communications explain orbital emphysema after nose blowing or sneezing and potential infection spread. The extraocular muscles guide a structured motility examination. Inferior rectus restriction often limits elevation after floor entrapment, but motility disturbance may also result from oedema, haemorrhage, muscle contusion, nerve palsy, pain or loss of fusion. CT evidence of muscle herniation alone does not prove clinical entrapment.

2. First priorities after orbital trauma

Follow the trauma primary survey first. Stabilize airway, breathing, circulation, haemorrhage, cervical spine and neurologic status. Check for traumatic brain injury, facial instability, penetrating injuries, airway compromise, severe epistaxis and associated chest/limb trauma. In significant facial trauma, protect the cervical spine until cleared. Orbital assessment must not delay care for a life-threatening injury.

History

• Ask what struck the face or eye, direction, force, speed, time and associated fall, crash, assault, sport, work activity, blast, projectile or penetrating object.
• Ask about vision change in each eye, colour desaturation, field loss, double vision, pain with eye movement, flashes, floaters, photophobia, nausea, vomiting, headache and loss of consciousness.
• Ask whether the patient blew the nose, sneezed, vomited or received pressure to the eye after injury. Ask about anticoagulants, bleeding disorders, prior ocular surgery or disease and contact lenses.
• In children, ask caregivers about behaviour and compare with baseline. A quiet-looking eye does not exclude an entrapped trapdoor fracture.

Focused examination when safe

1. Document visual acuity separately for each eye as early as feasible, with habitual correction. If a chart is unavailable, record counting fingers, hand movements, light perception or no light perception. Do not delay urgent treatment to complete a lengthy exam.
2. Inspect pupil size, shape and reactivity; test for a relative afferent pupillary defect with a swinging light test if safe. RAPD, dyschromatopsia or a new field defect can suggest optic-nerve or severe retinal injury.
3. Check extraocular movement in all directions, diplopia, pain on movement, ptosis and globe position (proptosis, enophthalmos or hypoglobus). Do not force the eye through painful restriction.
4. Look for lid laceration, ecchymosis, chemosis, subconjunctival haemorrhage, telecanthus, step-off, facial asymmetry, epistaxis, clear rhinorrhoea, crepitus and V1/V2 sensory changes.
5. Assess the globe and anterior segment only without pressure and only if open globe is not suspected. If open globe is possible, stop manipulation and apply a rigid shield.
6. Fundus examination, colour testing and formal visual fields may add information when safe and available; they must not postpone emergency decompression in clinically evident OCS.

3. Red flags requiring immediate escalation

4. Orbital proptosis and external signs

Proptosis (exophthalmos) may be non-pulsatile from orbital haemorrhage, oedema, emphysema, mass or displaced tissue. A pulsatile globe or bruit suggests vascular communication such as carotid-cavernous fistula, or rarely an orbital roof fracture with transmitted intracranial pulsation. These findings need urgent imaging and specialist review; do not compress the globe to test pulsation.

Telecanthus means increased distance between medial canthi, often from medial canthal tendon displacement in NOE injury. A palpable bony step, crepitus, facial numbness, cheek flattening, trismus or malocclusion points to fracture. Epistaxis can accompany nasal, midface or skull-base injury. Clear fluid from the nose after high-energy roof/cribriform trauma must be treated as possible CSF leak until assessed. Avoid blind nasal instrumentation or packing when skull-base injury is suspected; follow trauma/neurosurgical guidance.

5. Orbital fracture patterns and associated midface injuries

Le Fort fractures

Le Fort fractures describe horizontal, pyramidal or craniofacial separation patterns involving the maxilla and pterygoid plates. A Le Fort injury can coexist with orbital rim, floor, medial wall or skull-base injury. Clinically assess facial mobility only when appropriate, malocclusion, dental injury, midface swelling, epistaxis, airway risk and CSF leak. These are not simply isolated eye injuries. CT of the face/head and specialist maxillofacial/trauma review guide definitive care.

Orbital apex fracture and optic-nerve injury

The orbital apex contains the optic canal, superior orbital fissure and tightly grouped nerves and vessels. A fracture may damage the optic nerve, ocular motor nerves, V1, ophthalmic artery or cavernous-sinus communications. New severe visual loss, RAPD, ophthalmoplegia, ptosis, sensory deficit, CSF leak or pulsatile proptosis after high-energy trauma demands urgent specialist assessment and CT of the orbit/brain. A visual deficit can arise from direct nerve laceration/avulsion, canalicular compression, indirect traumatic optic neuropathy, retinal ischemia, globe injury or intracranial trauma; distinguish these where possible.

Orbital roof fractures

Roof injuries follow blunt or penetrating high-energy trauma and may extend into frontal sinus, frontal bone or anterior cranial fossa. Children may have a less developed frontal sinus, while older adults have different sinus anatomy; the mechanism and CT define risk. Findings include forehead/supraorbital rim depression, V1 numbness, ptosis, limitation of up-gaze, hypoglobus, proptosis, pulsation, epistaxis, CSF rhinorrhoea, anosmia or intracranial injury. Depressed fragments or a subperiosteal haematoma may displace the superior rectus/levator complex. Orbital roof repair decisions are individualized with ophthalmology, maxillofacial and neurosurgery. The source deck lists depressed skull fracture/anterior cranial-fossa compromise, significant diplopia or exophthalmos, and frontal sinus outflow-tract injury as operative concerns; this is not a bedside operative indication list for emergency clinicians.

Medial wall and naso-orbito-ethmoid fractures

NOE injuries occur when high-energy force strikes the central midface. They may involve the nasal process of the maxilla, lacrimal bone, ethmoid and medial orbital wall, with disruption of the medial canthal tendon, lacrimal drainage system or skull base. Type I has a central fragment bearing the canthal tendon; Type II has a comminuted central fragment with tendon attached to a segment; Type III has comminution or avulsion of the tendon attachment. Classification and repair planning are specialist tasks.

Look for depressed nasal bridge, telecanthus, medial canthal laxity/displacement, horizontal diplopia, enophthalmos, orbital emphysema, epistaxis, severe swelling, lacrimal injury and CSF rhinorrhoea. Complications include facial flattening, orbital haematoma, globe/brain injury, severe epistaxis, CSF leak and permanent canthal dystopia. Avoid nose blowing and advise sneeze with mouth open. Prophylactic systemic antibiotics are not automatically indicated for every closed orbital fracture; use local trauma, sinus and specialist guidance, especially for open/contaminated injury or infection.

Orbital floor blow-out fracture

An isolated floor blow-out fracture is a fracture of the orbital floor while the inferior orbital rim remains intact. A direct strike to the eye can transiently increase orbital pressure (hydraulic mechanism); a blow to the rim/cheek can transmit force and buckle the thin floor (buckling mechanism). Often the posterior medial floor is vulnerable. Orbital fat and sometimes muscle can herniate into the maxillary sinus. The term “blow-out” describes the bony pattern; it does not itself say that muscle is trapped or that surgery is required.

Symptoms include pain or diplopia on vertical gaze, infraorbital cheek/upper-lip numbness, swelling, bruising, nausea and vomiting. Signs can include restricted up-gaze or down-gaze, enophthalmos (sometimes more visible after oedema resolves), hypoglobus, hypaesthesia in V2 distribution, crepitus and orbital rim tenderness. Young children may have a minimally bruised “white-eyed” trapdoor fracture because elastic bone springs back and traps tissue. The child may have marked pain with eye movement, limitation of gaze, nausea/vomiting, bradycardia or syncope from the oculocardiac reflex. This is an urgent injury even if the eye looks white.

Restriction can be caused by entrapment, oedema, haemorrhage, muscle contusion or nerve injury. Entrapment is a clinical diagnosis, not merely a CT finding: patients with radiographic muscle herniation may move normally, while fat tethering can significantly restrict motion even when muscle stays in the orbit. Forced-duction testing is a specialist manoeuvre and is rarely necessary in an awake patient; do not force a painful eye to move in the ED.

Orbital emphysema

Air enters the orbit through a fracture communicating with an ethmoid or maxillary sinus, often after nose blowing, sneezing or Valsalva. Small emphysema can cause crepitus and swelling; increasing pressure may compress the optic nerve and threaten perfusion. Advise no nose blowing, sneeze with the mouth open, and avoid straining. If vision declines, proptosis becomes tense or an RAPD develops, treat as possible OCS and escalate immediately. Needle aspiration or orbital decompression is a specialist emergency procedure. Routine preventive antibiotics after every closed fracture are not supported uniformly; follow local policy and specialist advice.

Zygomaticomaxillary complex fracture

The zygoma functions as a facial buttress with articulations at the zygomaticomaxillary, zygomaticofrontal, zygomaticotemporal and posterior maxillary buttress regions. ZMC fracture may follow a moderate- or high-energy impact and often accompanies orbital floor or rim injury. Assess cheek projection, facial width, lateral canthus and lower-lid position, orbital rim step-off, infraorbital sensation, trismus, malocclusion and intraoral bruising in the upper gingivobuccal sulcus. Palpate gently after cervical-spine and globe safety are considered. Significant malar flattening, canthal/lid displacement, trismus/malocclusion, orbital enlargement, displacement or comminution may need repair. The maxillofacial team determines timing and fixation.

6. Orbital haemorrhage, orbital compartment syndrome and optic-nerve compression

Orbital haemorrhage may be intraconal (within the muscle cone), extraconal (outside the cone) or subperiosteal (between bone and periosteum). A confined orbit cannot expand freely. Blood or air can raise intraorbital pressure, compress the optic nerve and its vessels, and reduce retinal/optic-nerve perfusion. This produces orbital compartment syndrome. Vision can deteriorate rapidly, so management must be time-critical.

Recognize the syndrome clinically

• Rapid proptosis and tense eyelids/orbit, often with resistance to retropulsion assessed only by a clinician when open globe is excluded.
• Reduced visual acuity or colour vision, a new RAPD, visual field loss or progressive decline.
• Ophthalmoplegia or severely restricted movement, pain, tight swollen lids and chemosis.
• Raised IOP may support the diagnosis only when measuring it is safe and does not delay action. Never measure IOP when open globe is suspected.
• CT may show a retrobulbar haematoma or globe tenting, but a clear clinical OCS must not wait for imaging before treatment.

Do not rely on acetazolamide, mannitol, anterior-chamber paracentesis, cold packs or observation alone to treat acute OCS. They do not release the confined orbital compartment and may delay definitive decompression. These agents or procedures have specific indications in other eye conditions and must not replace the OCS response. The procedure carries risk, so it must be done by trained clinicians following local protocol and followed by definitive specialist management.

Separate orbital compartment syndrome from traumatic optic neuropathy

“Optic-nerve compression” may refer to pressure from retrobulbar blood/air in OCS or to a fracture fragment/mass at the apex/optic canal. Traumatic optic neuropathy (TON) is a broader nerve injury that may be direct (laceration, avulsion, displaced fragment) or indirect (transmitted force, stretching, contusion of the canalicular nerve). The external eye and early fundus can look normal in indirect TON. Findings include reduced acuity, colour desaturation, field defect and RAPD after head/orbit impact.

Urgently involve ophthalmology/neuro-ophthalmology, trauma and neurosurgery as indicated. Document serial visual acuity, pupils, colour vision, visual field symptoms and neurologic status. CT assesses fractures, bone fragments and haemorrhage; it cannot rule out all optic-nerve injury. MRI is considered only after metallic foreign body is excluded and when a specialist believes it will change management. Identify and relieve a demonstrable compressive lesion with specialist input. Evidence does not support routine megadose corticosteroids or routine optic-canal decompression for every indirect TON; high-dose steroids can harm patients with traumatic brain injury. Discuss any proposed treatment urgently with ophthalmology/neurosurgery and base it on the lesion, not on the phrase “optic-nerve compression” alone.

7. Imaging and investigations

• CT orbits/face without contrast: thin axial slices with coronal and sagittal reconstructions are the main initial study for orbital fractures, foreign bodies, haemorrhage and bone fragments. A combined CT head/face/cervical-spine plan may be required by the overall trauma mechanism.
• CT interpretation: review the orbital floor and walls, rim, apex/optic canal, globe contour, retrobulbar space, muscle position, maxillary/ethmoid sinuses, frontal bone and skull base. Clinical entrapment cannot be diagnosed from muscle herniation alone.
• CT angiography: consider when vascular injury or carotid-cavernous fistula is suspected, following trauma/neurovascular guidance.
• Visual assessment: acuity, pupils/RAPD, colour perception, motility and fields provide urgent functional information. Record a baseline and trend changes.
• Avoid unsafe procedures: no tonometry, forced retropulsion, pressure patch or ocular ultrasound if open globe has not been excluded. Do not delay OCS decompression to complete tests.
• Blood tests: guided by trauma, surgery and bleeding risk. Labs do not diagnose OCS or exclude optic neuropathy.

8. Intraorbital foreign bodies

An orbital foreign body may enter through the face or eyelid and remain in the orbit without entering the globe, or may traverse the orbit after perforating the globe. It can be missed when the external wound is small. Determine whether the globe is intact, assess for optic-nerve or muscle injury, look for infection and image the orbit. Metal, glass, wood, plant material, plastic, stone and other materials have different imaging and inflammatory profiles.

CT is usually initial imaging for suspected metallic, glass or orbital FB. Some wood or plastic is difficult to see; radiology and specialist review should consider material and scan timing. Do not perform MRI until ferromagnetic material has been excluded. Obtain cultures when there is infection, contamination or a specialist surgical reason; culture is not automatically required for every clean inert object. Removal versus observation depends on material, symptoms, accessibility, proximity to critical structures and the risk of surgery. This is a specialist decision, not a blanket rule to remove every object.

9. Emergency management at a glance

10. Orbital fracture repair: emergency versus planned

Not every radiographic fracture needs surgery. Emergency intervention is required for a threatened optic nerve or vision, severe orbital compartment pressure, acute haemorrhage, severe tissue/muscle entrapment—particularly in a child with oculocardiac reflex—or displaced fragments causing critical compression. These require immediate specialist review. Other fractures may be observed while swelling resolves and motility is reassessed.

For isolated floor fractures, specialist repair is considered for persistent diplopia that interferes with primary or functional gaze, clinically significant entrapment, troublesome enophthalmos/hypoglobus, a large defect with risk of late globe displacement, or a positive oculocardiac reflex. A size threshold such as half the floor or enophthalmos greater than 2 mm may inform decisions but is not a single automatic rule; symptoms, examination, CT, patient priorities and evolving oedema matter. Adult isolated floor fractures are often reassessed over 1–2 weeks if motility is improving, while severe entrapment, paediatric trapdoor fracture, oculocardiac reflex or vision-threatening compression cannot wait. Maxillofacial and ophthalmology teams decide timing.

Roof fractures may require repair for displaced/depressed fragments, neurologic or skull-base involvement, significant globe displacement/diplopia, or frontal sinus outflow injury. NOE injuries may require repair to restore medial canthal tendon position, lacrimal function, facial contour and stable central midface. ZMC fixation is considered for substantial cheek flattening, displacement, orbital-volume change, trismus or malocclusion. Emergency clinicians should document findings, protect the eye and expedite appropriate consultation rather than promise surgery or discharge based on a threshold alone.

11. Nursing assessment and care priorities

• Maintain trauma priorities and protect cervical spine; document mechanism, time, impact direction, loss of consciousness, anticoagulation and associated injuries.
• Record baseline visual acuity in each eye when safe, pupil findings/RAPD, colour change, motility, diplopia, proptosis/enophthalmos, pain, V1/V2 sensation and wound findings.
• Trend visual acuity, pupil responses, pain, proptosis, motility, consciousness, pulse and nausea/vomiting while awaiting definitive care.
• Watch for bradycardia, vomiting or syncope with eye movement in a child; report immediately because of possible oculocardiac reflex.
• For possible open globe, protect with rigid shield without pressure, discourage eating/drinking, rubbing, nose blowing and straining, and prepare for urgent transfer.
• Administer prescribed analgesia and antiemetics; avoid pressure or unprescribed eye drops. Keep the patient reassured and explain why repeated visual checks matter.
• Coordinate urgent transport, imaging and consultations; communicate acuity trend, RAPD, suspected open globe, entrapment, OCS signs and time of deterioration.
• Use teach-back for no nose blowing, shield care, return precautions, review appointments and activity restrictions at discharge.

12. Case-based application

Case 1: a child with a “white eye” after a ball strike

A 9-year-old has little bruising but severe vertical gaze pain, nausea and a pulse of 52/min after being hit near the eye. Up-gaze is restricted and vision is mildly blurred.

Interpretation: Do not dismiss this as a minor injury. A paediatric trapdoor fracture can trap orbital tissue while leaving little external bruising; nausea and bradycardia suggest oculocardiac reflex. Check acuity, pupils and associated trauma without forcing the eye. Obtain urgent CT and ophthalmology/maxillofacial consultation. Surgical release may be time-sensitive.

Case 2: rapidly progressive proptosis after blunt trauma

An adult develops a tense proptotic orbit and rapidly falling vision after a facial collision. The eye is difficult to move and an RAPD is present.

Interpretation: Suspect OCS. Rapidly assess whether open globe is suspected without pressing the eye. Activate ophthalmology/trauma and arrange immediate decompression by a trained credentialed clinician when indicated. Do not wait for CT or attempt to treat the compartment syndrome with acetazolamide or mannitol alone. Reassess vision and pupils after intervention.

Case 3: vision loss after head impact but normal-looking eye

A patient has reduced colour perception and a new RAPD after a high-energy head impact. The globe is intact and there is no tense proptosis; early fundus appearance is unremarkable.

Interpretation: Indirect TON is possible, as are intracranial, retinal or canal injuries. Document serial function, obtain urgent CT and involve ophthalmology/neuro-ophthalmology and trauma/neurosurgery. A normal early fundus does not exclude optic-nerve injury. Routine high-dose steroid or optic canal surgery is not evidence-based for every indirect injury; identify whether a surgically remediable compression exists.

Case 4: diplopia and cheek numbness after a punch

An adult reports double vision when looking up and numbness of the upper lip. There is infraorbital tenderness and lower-lid swelling.

Interpretation: Suspect orbital floor blow-out fracture with possible V2 injury. Check acuity, pupils, globe position and motility; exclude globe injury and OCS. Arrange thin-cut CT orbit/face and eye/maxillofacial review. Advise no nose blowing and sneeze with mouth open. CT herniation alone does not establish muscle entrapment or mandate surgery.

Case 5: high-energy central facial impact and telecanthus

A patient has a depressed nasal bridge, increased distance between medial canthi, tearing and clear fluid from the nose after a high-speed collision.

Interpretation: Suspect NOE fracture with medial canthal tendon/lacrimal injury and possible skull-base/CSF leak. Manage the trauma survey and cervical spine, avoid blind nasal packing or probing, document ocular function, obtain appropriate CT and urgently involve maxillofacial, ophthalmology and neurosurgical teams.

13. Knowledge check

1. Which seven bones form the orbit?
2. What differentiates an isolated orbital floor blow-out fracture from a rim fracture?
3. Why can a child with a trapdoor fracture have severe entrapment with little bruising?
4. Name four clinical findings that suggest orbital compartment syndrome.
5. What is the emergency decompression procedure for OCS, and who should perform it?
6. How does indirect traumatic optic neuropathy differ from orbital compartment syndrome?
7. Does muscle herniation on CT by itself prove clinical muscle entrapment?
8. Which sensory nerve is commonly affected in a floor fracture, and where is numbness felt?
9. What do telecanthus and medial canthal laxity suggest after high-energy trauma?
10. Why must an ED not wait for CT when there is clinically evident OCS?
11. What is the key advice for a patient with orbital emphysema or a sinus-communicating fracture?
12. Why are routine megadose steroids not recommended for every indirect traumatic optic neuropathy?

Answers

1. Frontal, sphenoid, zygomatic, maxilla, ethmoid, lacrimal and palatine.
2. A floor blow-out fracture breaks the orbital floor while the inferior rim remains intact.
3. Elastic paediatric bone can briefly open and recoil, trapping soft tissue in a “white-eyed” trapdoor injury.
4. Rapid vision loss, RAPD, tense lids/orbit, proptosis, ophthalmoplegia and chemosis are important signs.
5. Lateral canthotomy with inferior cantholysis; it should be performed by a trained, credentialed clinician under local protocol.
6. OCS is pressure-related compromise of optic nerve/retinal perfusion from a confined orbit; TON is direct or indirect injury to the nerve, which may occur without a tense orbit.
7. No. Entrapment is a clinical diagnosis; imaging must be interpreted with motility and symptoms.
8. Infraorbital nerve, V2; numbness can involve lower eyelid, cheek, upper lip, upper teeth and gingiva.
9. NOE fracture with medial canthal tendon displacement or avulsion.
10. Vision can be irreversibly lost quickly, and OCS is a clinical diagnosis requiring immediate pressure release.
11. Avoid nose blowing, sneeze with mouth open and avoid straining; worsening vision/proptosis needs emergency reassessment.
12. Available evidence has not shown routine benefit, and high-dose steroids may increase harm in traumatic brain injury.

Key takeaways

• Stabilize life-threatening trauma before a detailed eye examination, but recognize reversible vision threats quickly.
• Blow-out fracture often involves a thin floor with tissue herniation; diplopia, vertical movement pain and V2 numbness are common clues. Paediatric trapdoor injury may look deceptively mild.
• OCS is a time-critical clinical emergency: rapid vision loss, RAPD, proptosis, tense orbit and ophthalmoplegia require immediate specialist activation and trained decompression.
• “Optic-nerve compression” has more than one mechanism. Treat OCS differently from indirect traumatic optic neuropathy; routine megadose steroids or canal decompression for all TON is not supported.
• CT defines fracture anatomy and foreign bodies, but it must not delay decompression in clinically evident OCS and cannot alone diagnose muscle entrapment.
• Protect possible open globe with a rigid shield and avoid pressure or manipulation.
• Orbital roof, NOE, Le Fort and ZMC fractures may carry skull-base, brain, sinus, airway, lacrimal and facial-function complications that need multidisciplinary care.
• Do not blow the nose after sinus-communicating orbital fracture; instruct the patient to sneeze with the mouth open.

References and further reading

1. Panit Cherdchu. Orbital Trauma. Supplied 93-slide presentation, SlideShare.
2. American Academy of Ophthalmology EyeWiki. Orbital Floor Fracture.
3. American Academy of Ophthalmology EyeWiki. Pre-Ophthalmologist Management of Eye Trauma.
4. American Academy of Ophthalmology EyeWiki. Orbital Compartment Syndrome.
5. Royal Children’s Hospital Melbourne. Clinical Practice Guideline: Acute Eye Injury.
6. AO Foundation Surgery Reference. Orbital Floor Fracture Reconstruction: Emergency Treatment.
7. Blanch RJ, et al. Traumatic optic neuropathy management: a systematic review. Eye. 2024.
8. American Academy of Ophthalmology EyeNet. Orbital Compartment Syndrome.
9. American Academy of Ophthalmology EyeWiki. On-Call Ophthalmology: Orbital Fractures and Ocular Emergencies.