Residency · Residency · Emergency Medicine

Eye Emergencies: Acute Vision Loss, Chemical Burns, and Globe Rupture

Introduction

Ophthalmic emergencies require rapid diagnosis and intervention to preserve vision. While many eye complaints seen in the ED are benign, conditions such as chemical burns, open globe injuries, central retinal artery occlusion, and acute angle-closure glaucoma demand immediate treatment. The emergency physician must perform a focused ocular examination, identify vision-threatening conditions, initiate time-sensitive treatments, and arrange appropriate ophthalmologic consultation.

Focused Ocular Examination in the ED

Essential Components

Visual acuity is the "vital sign" of the eye and should be documented in every patient with an eye complaint using a Snellen chart or near card, with each eye tested individually with correction (a pinhole occluder can substitute when glasses are unavailable). Pupil examination assesses size, shape, and reactivity, and a relative afferent pupillary defect (RAPD or Marcus Gunn pupil) should be checked using the swinging flashlight test, as it indicates optic nerve or significant retinal pathology. External examination evaluates the lids, conjunctiva, cornea, and anterior chamber. Slit lamp examination assesses corneal integrity, anterior chamber depth and cell or flare, and lens position. Intraocular pressure is measured by tonometry (Tono-Pen, iCare, or Goldmann), with normal being 10 to 21 mmHg. Fundoscopy with a dilated exam using a direct ophthalmoscope or slit lamp with condensing lens evaluates the disc, macula, vessels, and retina. Fluorescein staining under blue or cobalt light illumination detects corneal epithelial defects.

Acute Vision Loss

Differential Diagnosis by Mechanism

Painless vision loss includes central retinal artery occlusion (CRAO), an acute, monocular, painless "eye stroke"; central retinal vein occlusion (CRVO) with subacute onset; retinal detachment with flashes, floaters progressing to a curtain or shadow; vitreous hemorrhage with sudden onset floaters or vision loss and an obscured fundus view; and ischemic optic neuropathy, where the anterior form is associated with giant cell arteritis in the elderly.

Painful vision loss includes acute angle-closure glaucoma with severe eye pain, halos around lights, nausea, and elevated IOP; optic neuritis with pain on eye movement, associated with multiple sclerosis; endophthalmitis, a post-surgical or post-traumatic intraocular infection with severe pain and hypopyon; and corneal ulcer or keratitis with severe pain, photophobia, and a white corneal infiltrate.

Central Retinal Artery Occlusion (CRAO)

CRAO is a time-critical emergency, as retinal tolerance for ischemia is approximately 90 to 120 minutes, analogous to acute stroke. Patients present with sudden, painless, monocular vision loss, with visual acuity often reduced to counting fingers or worse. Examination reveals an RAPD, a pale and edematous retina with a cherry-red spot at the macula (where the choroidal circulation is visible through the thin fovea), and "boxcar" segmentation of blood in retinal arterioles. The most common etiology is embolism from carotid atherosclerosis, though cardiac sources and giant cell arteritis are also responsible.

Emergency management includes emerging evidence for intra-arterial thrombolysis or IV tPA within 4.5 hours (based on limited evidence; discuss with ophthalmology and stroke team). Ocular massage with intermittent digital pressure on the globe (10 seconds on, 10 seconds off) may dislodge an embolus. IOP-lowering agents including timolol 0.5% drops, acetazolamide 500 mg IV, and anterior chamber paracentesis can reduce IOP to increase the perfusion gradient. Giant cell arteritis must be ruled out in patients over 50 with ESR, CRP, and platelet count; temporal artery biopsy should be arranged, and empiric high-dose steroids (methylprednisolone 1 g IV daily for 3 days) should be started if GCA is suspected to prevent contralateral eye involvement. The workup mirrors that of stroke: carotid duplex, echocardiography, and cardiac rhythm monitoring.

Retinal Detachment

Retinal detachment presents with sudden flashes (photopsia), floaters, and progressive visual field loss described as a curtain or shadow. Types include rhegmatogenous (from a retinal tear, the most common), tractional (diabetic), and exudative (inflammatory). Risk factors include high myopia, prior cataract surgery, trauma, and family history. Examination may reveal retinal folds, pigmented cells in the anterior vitreous ("tobacco dust"), and absent red reflex if the detachment is extensive. Management requires emergent ophthalmology consultation, with surgical repair (pneumatic retinopexy, scleral buckle, or vitrectomy) within 24 hours for macula-on detachments and urgent repair for macula-off.

Acute Angle-Closure Glaucoma

Patients present with severe unilateral eye pain, headache, nausea and vomiting, halos around lights, and blurred vision. Examination reveals conjunctival injection, a hazy and edematous cornea, a mid-dilated and fixed (non-reactive) pupil, IOP exceeding 40 mmHg (often 40 to 80 mmHg), and a shallow anterior chamber.

Emergency management aims to lower IOP immediately. Topical timolol 0.5% reduces aqueous production. Topical brimonidine 0.2% also reduces aqueous production. Topical pilocarpine 2% constricts the pupil and opens the trabecular meshwork but should be given only after IOP starts to drop, as at very high IOP the iris sphincter is ischemic and will not respond. Acetazolamide 500 mg IV or PO provides systemic reduction of aqueous production. Mannitol 1 to 2 g/kg IV is an osmotic agent for refractory cases. Definitive treatment is laser peripheral iridotomy performed by ophthalmology, and both eyes should be treated since the fellow eye is at risk.

<image>Fundoscopic comparison images showing: normal fundus on the left, central retinal artery occlusion with pale retina and cherry-red spot at the macula in the center, and acute angle-closure glaucoma with hazy cornea and mid-dilated fixed pupil on the right, with key diagnostic features labeled</image>

Chemical Burns

Classification and Urgency

Alkali burns are more dangerous than acid burns because alkali (NaOH, ammonia, lime, cement) penetrates deeply through liquefactive necrosis, while acid causes coagulative necrosis that limits penetration. Chemical burns are the one eye emergency where treatment precedes history and examination: irrigate first, ask questions later.

Immediate Management

Copious irrigation with the most readily available fluid (water, normal saline, or lactated Ringer's) should begin immediately. At least 1 to 2 liters per eye should be used, continuing for a minimum of 15 to 30 minutes. A Morgan lens enables continuous hands-free irrigation. Topical anesthetic (proparacaine or tetracaine) should be applied before irrigation to improve patient cooperation and enable lid retraction. The fornices should be swept with a moistened cotton swab to remove particulate matter such as lime or cement particles. pH should be checked before and after irrigation using litmus paper or pH strips, targeting 7.0 to 7.4, and irrigation should continue until pH normalizes and remains normal 5 minutes after stopping.

Roper-Hall Classification (Severity Grading)

Grade I involves corneal epithelial damage only with no limbal ischemia and a good prognosis. Grade II shows corneal haze but iris details are visible with less than one-third limbal ischemia. Grade III demonstrates total corneal epithelial loss, stromal haze obscuring the iris, one-third to one-half limbal ischemia, and a guarded prognosis. Grade IV presents with an opaque cornea and more than one-half limbal ischemia, carrying a very poor prognosis because limbal stem cell death prevents corneal re-epithelialization.

Post-Irrigation Management

A cycloplegic agent (cyclopentolate 1%) provides pain relief from ciliary spasm. Topical antibiotic (erythromycin ointment or fluoroquinolone drops) prevents infection. Oral analgesics and ascorbic acid at 500 mg PO four times daily promote collagen synthesis and corneal healing. Topical steroids should be avoided in the ED without ophthalmology guidance due to the risk of corneal melting. Ophthalmology consultation is indicated for all chemical burns Grade II and above, and all alkali burns warrant close follow-up.

Open Globe / Globe Rupture

Mechanism

Penetrating injury occurs when a sharp object enters the eye. Perforating injury involves an object entering and exiting through two wounds. Rupture occurs when blunt force causes globe wall failure at the weakest points, including the limbus, prior surgical sites, and equator.

Clinical Signs

The history involves high-energy trauma to the eye or orbit. Visual acuity is decreased, often severely. An irregular or teardrop-shaped pupil pointing toward the wound site indicates a peaked pupil. A shallow anterior chamber results from aqueous humor leak. A positive Seidel test shows streaming of aqueous humor through the wound when fluorescein is applied to the cornea, creating a dark stream within the fluorescein as leaking aqueous dilutes it. Subconjunctival hemorrhage extending 360 degrees suggests posterior rupture. Hypotony with IOP less than 5 mmHg may be found, though contact tonometry should not be used if globe rupture is suspected. Extruded intraocular contents including iris, vitreous, and lens may be visible.

Management

The eye should be protected with a rigid eye shield (metal or plastic Fox shield), and pressure or patching should not be applied. No examination requiring pressure on the globe should be performed, including tonometry, forced duction, and lid retraction against resistance. The patient should be made NPO, as surgical repair under general anesthesia will be required. Anti-emetics (ondansetron 4 mg IV) prevent Valsalva-induced extrusion of intraocular contents. Analgesics are provided for pain control. Tetanus immunization should be updated if not current. Systemic antibiotics including vancomycin 1 g IV plus ceftazidime 1 g IV (or moxifloxacin 400 mg IV for penicillin-allergic patients) prevent endophthalmitis. CT orbit with thin cuts and no contrast evaluates for intraocular foreign body and orbital fractures. MRI is contraindicated if a metallic foreign body is possible. Emergent ophthalmology consultation for surgical repair is essential.

<image>Cross-sectional anatomical illustration of an open globe injury showing the penetrating wound site, peaked pupil pointing toward the defect, shallow anterior chamber with aqueous leak, and iris prolapse through the wound, with a rigid eye shield properly positioned over the orbit without applying pressure to the globe</image>

Clinical Pearls

Chemical burns require immediate irrigation before any assessment. Alkali burns are worse than acid because alkali penetrates deeper. At least 1 to 2 liters should be used for irrigation, and pH should be checked until it normalizes. Central retinal artery occlusion is an "eye stroke," and IOP-lowering measures along with emergent ophthalmology and stroke team consultation should be considered. Giant cell arteritis must always be ruled out in patients over 50. Pressure should never be applied to a suspected open globe; a rigid shield should be used, anti-emetics given, IV antibiotics started, and ophthalmology consulted emergently. A mid-dilated, fixed pupil with severe eye pain, nausea, and elevated IOP is acute angle-closure glaucoma until proven otherwise, and IOP-lowering treatment should begin immediately. Visual acuity is the vital sign of the eye and should be documented in every patient with an ocular complaint before any intervention.

References

1. Bagheri N, Wajda BN, eds. The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease. 8th ed. Wolters Kluwer; 2022.
2. Hayreh SS, Zimmerman MB. "Central Retinal Artery Occlusion: Visual Outcome." American Journal of Ophthalmology. 2005;140(3):376-391.
3. Behrens-Baumann W. "Chemical Burns of the Eye." Ophthalmologe. 2018;115(11):911-916.
4. Kuhn F, et al. "The Birmingham Eye Trauma Terminology (BETT) System." Journal of Fr Ophtalmol. 2004;27(2):206-210.

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