Acute Angle-Closure Glaucoma
Acute angle-closure glaucoma is an ophthalmological emergency caused by sudden obstruction of aqueous outflow, presenting with severe eye pain, reduced vision, haloes, and a semi-dilated fixed pupil, requiring immediate IOP reduction.
Key Facts
Acute angle-closure glaucoma (AACG) is an ophthalmological emergency requiring immediate treatment to prevent permanent vision loss Presentation: severe unilateral eye pain, reduced vision, haloes around lights, nausea/vomiting, semi-dilated fixed pupil, injected eye, hazy cornea IOP is markedly elevated (often 40-80mmHg); eye feels "rock-hard" on palpation through closed lids Risk factors: hypermetropia (short eye), increasing age, female sex, East Asian ethnicity, shallow anterior chamber, family history Precipitants: pupil dilation (dim lighting, mydriatic drops, anticholinergics, sympathomimetics), prone position Emergency treatment: pilocarpine 2% drops (constricts pupil) + timolol 0.5% + IV acetazolamide 500mg + analgesia/antiemetic Definitive treatment: YAG laser peripheral iridotomy (creates alternative drainage pathway); treat BOTH eyes (prophylactic for fellow eye) Misdiagnosis: often misdiagnosed as migraine, acute abdomen, or stroke due to nausea/vomiting and headache
Overview
Key Facts
AACG causes rapid, irreversible optic nerve damage if not treated promptly. It should be considered in any patient presenting with a painful red eye and reduced vision.
Epidemiology
- Incidence: 12-15 per 100,000 per year (UK)
- Female:male ratio 3:1
- Peak age: >60
- East Asian ethnicity: significantly higher risk (smaller eyes, shallower anterior chambers)
- Hypermetropic (long-sighted) patients at higher risk
Aetiology
- Anatomically predisposed eye (short axial length, shallow anterior chamber, thick lens, narrow angle)
- Pupillary block: mid-dilated pupil causes iris to bow forward → blocks trabecular meshwork
- Precipitants: dim lighting, mydriatic drugs (tropicamide), anticholinergics (oxybutynin, TCAs, ipratropium), sympathomimetics
Pathophysiology
- Pupillary block → iris bows forward → peripheral iris occludes trabecular meshwork → sudden cessation of aqueous outflow → rapid IOP rise (40-80mmHg) → corneal oedema (haze) → optic nerve ischaemia → retinal ganglion cell death
Clinical Presentation
Symptoms
- Severe unilateral eye pain (often frontal/periorbital)
- Reduced/blurred vision
- Haloes around lights (corneal oedema causes light diffraction)
- Nausea and vomiting (vagal response to pain; can mimic acute abdomen)
- Headache (can mimic migraine or stroke)
- Profuse lacrimation
Signs
- Red eye (mixed conjunctival and ciliary injection)
- Hazy/oedematous cornea (steamy)
- Semi-dilated, fixed (non-reactive) pupil — oval shaped
- Rock-hard eye (elevated IOP palpable through closed lids)
- Shallow anterior chamber (by slit lamp or pen torch — narrow shadow sign)
- IOP markedly elevated (often 40-80mmHg)
Red Flags
- This IS a red flag — any presentation matching above requires emergency management
- Fellow eye may have narrow angles (at risk of same episode)
- Misdiagnosis risk: nausea/vomiting → "acute abdomen"; headache → "migraine"
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Anterior uveitis | Miosis, ciliary flush, cells/flare, normal IOP | Slit lamp |
| Keratitis | Corneal opacity, fluorescein uptake, normal IOP | Slit lamp |
| Migraine | Headache, visual aura, normal eye examination | Clinical |
| Cluster headache | Periorbital pain, lacrimation, conjunctival injection | Clinical |
| Phacomorphic glaucoma | Mature cataract, shallow AC | Slit lamp, B-scan |
Diagnosis / Investigation
Bedside
- Visual acuity (usually significantly reduced)
- IOP measurement (Goldmann tonometry): markedly elevated; if not available, palpation through closed lids (very firm)
- Pen torch: semi-dilated, oval, fixed pupil; shallow AC (narrow shadow sign)
- Slit lamp: corneal oedema, shallow AC, closed angle (gonioscopy when acute phase resolved)
Bloods
- Not needed for diagnosis
- U&Es if acetazolamide being used (electrolyte disturbance)
Imaging
- Anterior segment OCT/ultrasound biomicroscopy: angle assessment (specialist)
- B-scan ultrasound: if no view of posterior segment
Special Tests
- Gonioscopy: gold standard for angle assessment (performed after acute phase resolved)
- Fellow eye gonioscopy: assess for narrow angles (prophylactic iridotomy needed)
Management
Emergency Treatment (Reduce IOP)
- Lie patient supine (iris falls back, may partially open angle)
- Pilocarpine 2% drops to affected eye: every 5 minutes × 3 then 4× daily (constricts pupil → opens angle)
- Pilocarpine to fellow eye also (prophylactic)
- Timolol 0.5% drops to affected eye: single dose (reduces aqueous production)
- IV acetazolamide 500mg STAT (reduces aqueous production; oral 250mg QDS maintenance)
- Topical steroid (dexamethasone 0.1%): reduces inflammation from acute episode
- Analgesia: paracetamol ± opioid
- Antiemetic: cyclizine 50mg IM/IV
- If IOP not responding: IV mannitol 20% (1g/kg over 20 minutes) — osmotic diuretic
- Pilocarpine may not work if IOP >50mmHg (sphincter ischaemia); must reduce IOP first with systemic agents
Definitive Treatment
- YAG laser peripheral iridotomy (PI): creates small hole in peripheral iris → bypasses pupillary block → allows aqueous flow to trabecular meshwork
- Performed once cornea has cleared (usually within 24-48 hours)
- Both eyes treated (fellow eye prophylactic iridotomy — essential)
- Lens extraction (cataract surgery): removes the thick lens contributing to crowding; increasingly used as primary or early treatment
Surgical/Interventional
- Surgical peripheral iridectomy: if laser not possible
- Lens extraction: if angle-closure recurs despite PI or coexisting cataract
- Goniosynechialysis: to break peripheral anterior synechiae (specialist)
Referral Criteria
- AACG: immediate ophthalmology referral (same day/emergency)
- Fellow eye: prophylactic iridotomy arranged urgently
- Post-acute: ongoing glaucoma monitoring
Prognosis
- Prompt treatment (within hours): good visual prognosis; IOP reduces within hours of treatment
- Delayed treatment: permanent optic nerve damage; visual field loss; blindness
- After laser PI: recurrence is rare; fellow eye protected
- Chronic angle-closure may develop if repeated/prolonged episodes with synechiae formation
- Risk of further episodes in fellow eye is 40-80% without prophylactic treatment
Other Relevant Information
Emergency AACG Treatment Summary
| Step | Treatment |
|---|---|
| 1 | Lie supine |
| 2 | Pilocarpine 2% drops (both eyes) |
| 3 | Timolol 0.5% drops |
| 4 | IV acetazolamide 500mg |
| 5 | Topical steroid |
| 6 | Analgesia + antiemetic |
| 7 | If refractory: IV mannitol |
| 8 | Definitive: YAG laser PI (both eyes) |
Risk Factors for Angle-Closure
| Factor | Mechanism |
|---|---|
| Hypermetropia | Short eye, shallow AC |
| Female sex | Smaller eyes |
| Age >60 | Lens thickens with age |
| East Asian ethnicity | Anatomically narrow angles |
| Family history | Anatomical predisposition |
| Anticholinergic drugs | Pupil dilation |