Ophthalmological emergencies — chemical burns, acute angle closure, central retinal artery

ACEM Fellowship Learning Objective ACEMF-3.5-TS2-2.1

Overview: ED Approach to Ocular Presentations

Undifferentiated eye presentations demand a structured framework. Key triage concerns are vision-threatening emergencies (requiring immediate action) versus non-vision-threatening conditions requiring analgesia, treatment, and appropriate follow-up. Every ocular complaint warrants formal visual acuity testing before any intervention, slit-lamp examination where available, and intraocular pressure (IOP) measurement when indicated. Normal IOP is 10-21 mmHg.

Eyelid and Lacrimal Pathology

Blepharitis

Aetiology: Chronic inflammation of the eyelid margins. Two main subtypes:

• Anterior blepharitis, Staphylococcal infection or seborrhoeic dermatitis affecting lash follicles
• Posterior blepharitis, Meibomian gland dysfunction (MGD), the more common form, causing abnormal lipid secretion and altered tear film stability

Pathophysiology: Meibomian glands produce the outermost lipid layer of the tear film. Obstruction or bacterial lipase activity (predominantly Staphylococcus aureus, S. epidermidis) degrades meibum into irritant free fatty acids, causing lid margin inflammation, tear film instability, and secondary dry eye. Chronic colonisation promotes biofilm formation, perpetuating the inflammatory cycle.

ED relevance: Not a vision-threatening emergency. Presents with lid crusting, burning, and foreign-body sensation. ED role is to exclude more serious pathology (e.g. preseptal cellulitis) and initiate lid hygiene advice. Complications include chalazion, hordeolum, and keratitis.

Dacryocystitis

Aetiology: Infection of the lacrimal sac, most commonly following obstruction of the nasolacrimal duct. Causative organisms include Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae.

Pathophysiology: Nasolacrimal duct obstruction (congenital stenosis, nasal polyps, trauma, or chronic dacryostenosis) causes stasis of tears and mucus within the lacrimal sac. This creates an ideal environment for bacterial proliferation, leading to abscess formation within the sac and surrounding soft tissue cellulitis. Acute dacryocystitis manifests as painful, erythematous swelling at the medial canthal region inferior to the medial canthus, this distinguishes it from preseptal orbital cellulitis arising superiorly. Orbital spread is a rare but serious complication.

ED relevance: Requires systemic antibiotics (oral or IV depending on severity). Fluctuant abscesses may require incision or ophthalmology review.

Conjunctiva

Conjunctivitis

Aetiology and Pathophysiology:

Gonococcal conjunctivitis is a sight-threatening emergency, hyperpurulent discharge with corneal penetration risk; requires urgent ophthalmology and systemic antibiotics (IV ceftriaxone 1-2 g). Neonatal conjunctivitis within 5 days of birth suggests chemical (silver nitrate) or gonococcal cause; after 5-14 days suggests chlamydia.

Spontaneous Subconjunctival Haemorrhage

Aetiology: Rupture of small conjunctival vessels. Precipitants include Valsalva (coughing, sneezing, vomiting), trauma, hypertension, anticoagulation, bleeding diatheses, and contact lens wear.

Pathophysiology: The conjunctival vessels lack the robust supporting connective tissue of deeper structures. Sudden pressure elevation or fragility causes extravasation beneath the transparent conjunctiva, producing a vivid red patch that is self-limiting and resolves over 1-2 weeks. Vision is unaffected. The key ED decision is to rule out haemorrhagic conditions, check blood pressure, and consider anticoagulation review. Bilateral or recurrent subconjunctival haemorrhage without obvious trigger warrants coagulation screen.

Corneal Pathology

Corneal Abrasions

Pathophysiology: The corneal epithelium is 5-6 cell layers thick and has a rich sub-basal nerve plexus, explaining the severe pain. Disruption of the epithelium exposes nerve endings and creates risk of secondary infection. The epithelium regenerates rapidly (24-72 hours for small abrasions). Large abrasions or those from contact lenses carry greater infection risk and risk of recurrent erosion syndrome.

ED management principles: Topical anaesthetic for examination only (never prescribe for home use, impairs epithelial healing and masks progression). Topical NSAIDs or lubricants for analgesia. Patching is not recommended routinely. Contact-lens-related abrasions: treat empirically for Pseudomonas (topical fluoroquinolone). Recurrent erosion is caused by failure of epithelial hemidesmosome reattachment to the basement membrane.

Corneal Ulcers

Aetiology: Bacterial (Pseudomonas aeruginosa, Staphylococcus, Streptococcus), viral (HSV dendritic ulcer, HSV disciform keratitis), fungal (Fusarium, Candida, often post-trauma with organic matter or contact lens), and acanthamoeba (contact lens wearers in contaminated water).

Pathophysiology: Full-thickness epithelial defect with underlying stromal infiltration and inflammatory cell recruitment. Stromal proteases from both bacteria and host neutrophils cause progressive tissue destruction. Untreated, this can perforate the globe. HSV dendritic ulcers result from viral replication within epithelial cells, producing characteristic branching lesions visible with fluorescein and cobalt blue light; deeper HSV disciform keratitis is an immune-mediated endothelial/stromal reaction to viral antigen. Topical steroids are contraindicated in dendritic HSV but may be used cautiously (with antiviral cover) in disciform disease, an ophthalmology decision.

ED red flags: Corneal ulcer with hypopyon (pus in anterior chamber) indicates severe bacterial or fungal infection. This is a same-day ophthalmology emergency.

Ocular Foreign Bodies

Superficial foreign bodies lodge in the tarsal conjunctiva or cornea. Most are metallic and industrial. Corneal metallic foreign bodies develop a rust ring from oxidation within 24-48 hours, requiring removal with a needle or burr under slit lamp.

Intraocular foreign bodies (IOFB): Penetrating injuries may be subtle, a small entry wound with a dramatic mechanism (grinding, hammering metal on metal) should prompt consideration of IOFB. Seidel's test (fluorescein streaming at a wound site from aqueous humour leakage) confirms open globe. If open globe is suspected: do not apply pressure, shield the eye, keep patient nil by mouth, administer tetanus prophylaxis, anti-emetics, and arrange urgent ophthalmology. CT orbits is the investigation of choice, MRI is contraindicated if ferromagnetic IOFB is possible.

Ocular Burns

Roper-Hall classification grades chemical burns I-IV based on corneal clarity and limbal ischaemia. Grade IV (total limbal ischaemia, opaque cornea) carries the worst prognosis. Irrigation is the single most important intervention, begin before formal assessment, using any available neutral fluid. One litre per eye, at minimum 20-30 minutes, checked by pH measurement in the inferior fornix.

Glaucoma

Acute Angle-Closure Glaucoma (AACG)

Pathophysiology: Aqueous humour is produced by the ciliary body, flows through the pupil, and drains via the trabecular meshwork at the iridocorneal angle into Schlemm's canal. In eyes with narrow anterior chamber angles (hypermetropes, increasing lens size with age, certain ethnicities), pupil mid-dilation causes the iris to bow anteriorly (pupillary block), occluding the angle and causing acute IOP elevation, often >40-50 mmHg.

Elevated IOP compresses the optic nerve head microvasculature, threatening irreversible visual loss within hours. Corneal oedema at high IOP produces halos around lights and accounts for the "steamy" corneal appearance.

ED presentation: Acute severe headache, nausea/vomiting, unilateral red eye, fixed mid-dilated pupil (4-6 mm), markedly reduced visual acuity, rock-hard globe. Can mimic acute neurological or GI emergencies, always check pupils in headache patients.

Immediate management:

• IOP-lowering: topical timolol 0.5% + apraclonidine + pilocarpine 2% (to constrict pupil and open angle)
• Systemic: acetazolamide 500 mg IV + IV analgesia/anti-emetics
• Definitive: laser peripheral iridotomy by ophthalmology

Uveitis

Aetiology: Anterior uveitis (iritis/iridocyclitis), HLA-B27-associated conditions (ankylosing spondylitis, reactive arthritis, IBD-related, psoriatic arthritis), sarcoidosis, HSV, CMV. Posterior uveitis (choroiditis, retinitis), toxoplasmosis, CMV retinitis (immunocompromised), sarcoidosis, TB.

Pathophysiology: Breakdown of the blood-aqueous or blood-retinal barrier allows inflammatory cell infiltration. Protein leak into the aqueous produces "flare" (Tyndall effect on slit lamp, likened to a headlight beam in dusty air). Cellular exudate produces keratic precipitates on the corneal endothelium. Posterior synechiae (iris-lens adhesions) can cause pupil irregularity and, if circumferential (seclusio pupillae), can precipitate secondary angle-closure.

ED assessment: Perilimbal (ciliary) flush, small/irregular pupil, photophobia, decreased vision, aching pain. Distinguish from conjunctivitis (which does not cause photophobia or ciliary flush) and AACG (which has a dilated pupil and higher IOP). Anterior uveitis is commonly managed with topical steroids (prednisolone acetate 1%) and a cycloplegic agent (cyclopentolate 1%) to prevent synechiae and reduce ciliary spasm.

Retinal Detachment

Pathophysiology: Three mechanisms:

1. Rhegmatogenous (most common), full-thickness retinal break allows liquefied vitreous to track under the neurosensory retina, separating it from the retinal pigment epithelium (RPE). Associated with myopia, posterior vitreous detachment, trauma.
2. Tractional, fibrovascular membranes (diabetic retinopathy, sickle cell) mechanically pull the retina away from RPE. No retinal break.
3. Exudative/serous, fluid accumulation under retina from severe hypertension, malignancy, inflammatory conditions. No break or traction.

ED presentation: Photopsia (flashes, vitreoretinal traction stimulating photoreceptors), floaters (vitreous syneresis or vitreous haemorrhage), then a visual field defect ("curtain" or "shadow") progressing toward central vision. Macula-on detachment preserves acuity; macula-off detachment causes dramatic central vision loss and is more urgent.

ED action: Same-day/next-day ophthalmology review (macula-on may allow planned theatre); macula-off requires urgent surgery within hours to days. Point-of-care ultrasound can identify retinal detachment in a closed/painful eye (hyperechoic membrane anchored at the optic disc).

Vascular Ocular Emergencies

Central Retinal Artery Occlusion (CRAO)

Pathophysiology: The retina tolerates ischaemia poorly, irreversible photoreceptor damage begins within 90-100 minutes of complete CRAO (though the choroidal circulation supplies the outer retina, offering some protection to photoreceptors). Embolism (carotid atherosclerosis, cardiac, amaurosis fugax if transient), thrombosis in situ, vasospasm (rare), or vasculitis (giant cell arteritis, GCA) causes sudden, painless, profound unilateral visual loss. Fundoscopy shows a pale, oedematous retina with a cherry-red spot at the fovea (where the choroidal circulation is visible through the thin foveal tissue).

ED management: Treat as an ocular stroke, time-critical within 4-6 hours. GCA must be excluded immediately (ESR, CRP, temporal artery tenderness); if suspected, administer high-dose corticosteroids before biopsy. Lower IOP to encourage embolic dislodgement: ocular massage (sustained digital pressure 15 seconds on/off), acetazolamide, timolol. Anterior chamber paracentesis is a specialist procedure. Arrange urgent CT/MR angiography (30% have concurrent cerebral ischaemia, refer to stroke pathway).

Central Retinal Vein Occlusion (CRVO)

Pathophysiology: Compression of the central retinal vein at the lamina cribrosa (often by an adjacent sclerotic central retinal artery) causes venous hypertension, increased capillary hydrostatic pressure, and breakdown of the inner blood-retinal barrier. This leads to diffuse retinal haemorrhages ("blood and thunder" fundus, flame haemorrhages in all four quadrants), disc oedema, dilated tortuous veins, and macular oedema (the primary cause of vision loss). Ischaemic CRVO (capillary non-perfusion >10 disc areas) carries high risk of neovascularisation and neovascular glaucoma (rubeosis iridis). Risk factors: hypertension, hyperviscosity, glaucoma, thrombophilia.

ED action: Urgent ophthalmology referral. Investigate for systemic vascular risk factors (BP, lipids, glucose, FBC, coagulation). Anti-VEGF injections are the mainstay of treatment for macular oedema; neovascular complications require panretinal photocoagulation.

ACEM Fellowship Implications

High-Yield Viva Points

OSCE Approach to Eye Examination

1. Visual acuity (Snellen chart), always before any intervention
2. External inspection, lids, periorbital, proptosis
3. Pupil reactions, RAPD indicates posterior segment or optic nerve pathology
4. Slit-lamp biomicroscopy, anterior segment, fluorescein staining
5. IOP measurement, Goldmann/Tono-Pen/iCare
6. Fundoscopy, posterior segment (often dilate after IOP checked and AACG excluded)

Disposition Framework

Steroid Use in ED Eye Presentations

Topical glucocorticoids are predominantly an ophthalmology-initiated therapy. Emergency physicians should understand that steroids are used for anterior uveitis, post-chemical burn inflammation, allergic eye disease, and postoperative inflammation. Agents include prednisolone acetate 1% (potent, anterior segment penetration), dexamethasone 0.1%, fluorometholone (lower IOP-raising risk), and loteprednol (lowest systemic absorption). Critical contraindications relevant to ED: HSV dendritic ulceration, fungal keratitis, active bacterial infection without antimicrobial cover. Steroid-induced IOP elevation and posterior subcapsular cataract are well-recognised complications of prolonged use, not an ED concern acutely, but relevant when counselling patients.

POCUS in Ocular Emergencies

Point-of-care ultrasound (linear probe, 10-15 MHz, gel on closed eyelid) can identify:

• Retinal detachment, hyperechoic membrane anchored at optic disc
• Vitreous haemorrhage, diffuse echogenicity without membrane attachment
• Lens dislocation, IOFB, vitreous detachment
• Optic nerve sheath diameter $>5$ mm suggests raised intracranial pressure (though this is an indirect sign with moderate sensitivity)

Sources

• ACEM policy documents
• Therapeutic Guidelines (eTG)