Initial evaluation of ocular trauma is often performed by non-ophthalmologists such as emergency physicians, general internists, and primary care physicians. A systematic approach allows early identification of vision-threatening conditions and optimizes prognosis.
The basic principle of triage is two-tiered: first, prioritize life-threatening conditions (e.g., intracranial injury, airway obstruction), then address vision-threatening conditions. Appropriate initial management before referral to an ophthalmologist directly impacts visual prognosis.
Epidemiological features of ocular trauma are as follows:
Ocular trauma is broadly classified into mechanical and non-mechanical trauma. Mechanical trauma is further classified into mechanical injuries (open-globe and closed-globe). Checking vital signs (consciousness, respiration, blood pressure, pulse, temperature) is an essential part of the initial assessment.
In the United States in 2008, approximately 640,000 emergency department visits (209 per 100,000 population) were due to eye injuries. 44.6% of injuries occurred at home, and contusions or corneal abrasions accounted for 44.4% of all cases.
The main clinical findings to be assessed during the initial evaluation are shown below.
Findings of Open Globe Injury
Findings of Closed Globe Injury
Neurological Findings
Orbital findings
Other important findings
The mechanisms of ocular trauma are diverse, and the pathology and prognosis vary greatly depending on the type of injury.
Open Globe Injury
Definition: Full-thickness wound of the cornea or sclera.
Laceration (sharp external force): There are three types: penetrating injury (single wound), perforating injury (entry + exit), and intraocular foreign body (IOFB).
Rupture (blunt external force): Occurs due to a sudden rise in intraocular pressure. It often results in a scleral wound parallel to the limbus, and diagnosis may be delayed because it is covered by conjunctiva and Tenon’s capsule.
Closed Globe Injury
Definition: Injury without a full-thickness wound.
Contusion: Damage to the eyeball and surrounding tissues caused by blunt force. It can cause hyphema, lens subluxation, retinal detachment, etc.
Lamellar laceration: Partial-thickness corneal or scleral laceration that does not extend through the full thickness.
The Birmingham Eye Trauma Terminology (BETT) and the Globe and Adnexal Trauma Terminology are used as classification systems. 1)
The injury site is classified into the following three zones. 1)
| Zone | Extent | Characteristics |
|---|---|---|
| Zone I | Cornea to limbus | Limited to the cornea |
| Zone II | Limbus to 5 mm posterior to the sclera | Includes the anterior sclera |
| Zone III | More than 5 mm posterior to the sclera | Posterior sclera and perioptic area |
Main causes of blunt trauma: Sports (baseball, golf, boxing, soccer, etc.), traffic accidents (airbags), falls, fireworks.
Causative agents and mechanisms of chemical trauma: Alkalis saponify fatty acids, causing liquefactive necrosis and penetrating deep into tissues. When they reach the limbal stem cells, healing is severely impaired. Acids cause coagulative necrosis due to protein denaturation, forming a barrier that limits deep penetration. Therefore, alkali injuries are generally more severe.
Risk of orbital fracture in young patients: In children with highly elastic bones, the risk of extraocular muscle entrapment is high, often leading to a surgical emergency.
Generally, alkali is more severe. Alkali causes liquefactive necrosis, penetrates deeply, and when it reaches the limbal stem cells, healing is impaired. Acid forms a barrier via coagulative necrosis that limits penetration, but at high concentrations it can also cause severe damage.
A systematic initial evaluation determines the visual prognosis.
Perform only after open globe injury has been ruled out. Normal range is 11–21 mmHg.
The following tests are combined for diagnosis.
Classification according to urgency and key points of initial management.
Orbital compartment syndrome
Urgency: Ultra-emergency (permanent vision loss within 90 minutes)
Procedure: Emergency decompression via lateral canthotomy and inferior cantholysis. Decision based on clinical diagnosis; immediate procedure required.
Open globe injury
Urgency: Emergency (prompt ophthalmology referral)
Procedure: Avoid maneuvers that increase intraocular pressure. Protect with eye shield (no pressure on the globe). Defer foreign body removal. Administer antiemetics and analgesics, NPO, elevate head 30 degrees. Midazolam can provide sedation without increasing intraocular pressure. Administer broad-spectrum antibiotics and check tetanus immunization.
Chemical trauma
Urgency: Semi-emergency (immediately start irrigation)
Procedure: Instruct irrigation with at least 500 mL of running water before arrival. After arrival, continuous irrigation with isotonic saline or lactated Ringer’s solution until pH reaches 7.0–7.4. Use Morgan lens if blepharospasm occurs. Remove residual foreign bodies in the fornix as they may prevent pH stabilization.
Hyphema
Urgency: Semi-emergency (ophthalmologic evaluation needed)
Procedure: Elevate head of bed 30–45 degrees, apply eye shield, rest. Avoid NSAIDs and aspirin due to increased bleeding risk from platelet inhibition. Discuss risks and benefits of discontinuing anticoagulation with the internist.
Acute management and surgical indications are as follows.
In Japan, the basic policy is to wait for natural absorption with rest. Hospitalization is recommended for children or when the hyphema level exceeds 1/3 to 1/2 of the anterior chamber.
| Medication | Dosage |
|---|---|
| Atropine ophthalmic solution (1%) | Once daily at bedtime |
| Rinderon ophthalmic solution (0.1%) | Four times daily |
| Adona tablets (30 mg) | 3 tablets, 3 times a day after meals |
| Timoptol eye drops (0.5%)* | 2 times a day (when intraocular pressure is elevated) |
Diagnosis should be made within 24–48 hours after injury. The effectiveness of treatment options is controversial.
Immediately refer to an ophthalmologist.
The orbit is a closed space; acute hemorrhage or soft tissue swelling can rapidly increase intraorbital and intraocular pressure. If this exceeds the arterial perfusion pressure of the optic nerve, permanent vision loss can occur within 90 minutes. Emergency decompression via lateral canthotomy and inferior cantholysis is the only effective treatment.
Aspirin and NSAIDs inhibit platelet function and increase the risk of rebleeding. In the acute phase of hyphema, these medications must be avoided; if analgesia is needed, acetaminophen is preferred.
Alkalis saponify fatty acids, causing liquefactive necrosis and penetrating deep into the cornea. When they reach the limbal stem cells, epithelial regeneration is impaired. Acids form a barrier through coagulative necrosis due to protein denaturation, self-limiting deep penetration.
Ocular contusion causes anteroposterior compression and equatorial expansion, damaging the “seven rings of trauma.” Blunt force increases intraocular pressure, stretching the limbus, causing aqueous humor to move posteriorly and into the angle, damaging iris and ciliary body vessels and leading to bleeding.
Acute hemorrhage or soft tissue swelling within the confined orbital space rapidly increases orbital pressure and intraocular pressure. When this exceeds the arterial perfusion pressure of the optic nerve, permanent vision loss can occur within 90 minutes.
Two mechanisms combine. The buckling theory involves force transmitted through bone causing wall failure; the hydraulic theory involves force transmitted through the eye, increasing intraocular pressure and causing wall failure. In young patients, higher bone elasticity makes the orbital wall less likely to fracture, so entrapment of extraocular muscles (greenstick fracture type) is more common than open fractures.
Ocular contusion causes compression followed by anteroposterior rebound decompression, leading to vitreous traction on the retina and tear formation. Trauma liquefies the vitreous, and liquefied vitreous accumulates under the retina through the tear, causing detachment. In open globe injuries, direct retinal laceration or secondary traction from incarcerated vitreous gel is the main mechanism. In closed globe injuries, large retinal tears at the vitreous base due to blunt force are characteristic.
Direct traumatic optic neuropathy (rare): a penetrating object directly damages the optic nerve. Indirect traumatic optic neuropathy: blunt trauma causes deformation of the optic canal → shearing of the optic nerve → swelling → compression of the neurovascular bundle → worsening ischemia.
A rare but serious complication in which exposure to neoantigens after trauma triggers bilateral granulomatous uveitis.
McMaster et al. (2025) conducted a systematic review and meta-analysis of 16 studies involving 10,874 eyes. 1) Primary repair within 24 hours was shown to reduce the risk of endophthalmitis compared to repair after 24 hours. Evidence is particularly strong for penetrating injuries and intraocular foreign body (IOFB) injuries. Regarding visual prognosis, heterogeneity among studies was high, and the evidence level was downgraded to “very low.” For the effect of IOFB removal timing on endophthalmitis rate, 4 studies with 2,216 cases were analyzed, but only one study reported a significant association.
Kheir et al. (2021) reported ocular trauma in 39 patients (48 eyes) from the Beirut port explosion. 2) Injuries were predominantly shrapnel-based, and 53.8% required surgical intervention. Final best-corrected visual acuity worse than 20/200 occurred in 14.5% (7 eyes), and all 4 eyes with no light perception required enucleation or evisceration. The study emphasizes the importance of comprehensive ocular trauma management strategies in mass casualty disasters.
