Presentation
- Sudden-onset severe unilateral eye pain, headache, blurred vision, coloured halos around lights, nausea and vomiting — the systemic symptoms can mimic an acute abdomen or migraine and delay diagnosis.
- Often occurs in dim illumination (e.g., a dark theatre, evening hours) due to physiologic pupillary dilation.
- Risk profile: hyperopia, shallow anterior chamber, family history of angle closure; certain ethnic groups (higher reported prevalence in Asian populations) are more predisposed.
- Can be precipitated by pupil-dilating medications — anticholinergics, sympathomimetics, topiramate, and certain antihistamines/antidepressants.
Findings
★ Signature Finding
Markedly elevated IOP (commonly 40–80 mmHg) with a mid-dilated, fixed, poorly reactive pupil. Mechanism: pupillary block prevents aqueous flow from the posterior to anterior chamber, causing iris bombé and appositional closure of the drainage angle.
- Corneal microcystic oedema/haze, conjunctival injection (ciliary flush), shallow anterior chamber, and a closed angle on gonioscopy.
- The fellow eye typically also has a narrow angle — roughly 80% of such fellow eyes are reported at risk of a similar attack.
Etiology & Mechanism
- Primary: pupillary block in an anatomically predisposed eye (shallow anterior chamber, short axial length, anteriorly positioned/thick lens, hyperopia).
- Secondary/non–pupillary block mechanisms: lens-related (phacomorphic), drug-induced (e.g., topiramate causing ciliary body oedema and anterior rotation), neovascular glaucoma with angle closure, uveitic disease with posterior synechiae, and plateau iris syndrome.
Red Flags — Do Not Miss
Critical — Do Not Miss
- IOP not responding to initial medical therapy — risk of irreversible optic nerve damage within hours; escalate promptly (paracentesis, urgent laser or surgical iridotomy/iridectomy).
- A narrow angle in the fellow eye — schedule prophylactic laser peripheral iridotomy given the substantial reported risk of a future attack.
- Persistent corneal oedema preventing laser iridotomy — consider topical glycerin to temporarily clear the cornea, or proceed to surgical iridectomy/lensectomy.
Investigations
- IOP measurement (Goldmann applanation preferred) and gonioscopy of BOTH eyes to confirm angle closure and identify secondary mechanisms.
- B-scan ultrasound or ultrasound biomicroscopy/AS-OCT if a non–pupillary-block mechanism (choroidal effusion, ciliary body rotation) is suspected.
- Dilated fundus exam (once IOP is controlled) to assess the optic nerve.
Management
- ① Immediate combination topical therapy — a topical beta-blocker, an alpha-2 agonist, and a topical or oral carbonic anhydrase inhibitor — to begin lowering IOP.
- ② Pilocarpine added once IOP has come down enough for the ischemic iris sphincter to respond.
- ③ If response is inadequate: oral or IV acetazolamide (commonly cited dose: 500 mg) and/or IV mannitol (commonly cited dose range: 1–2 g/kg).
- ④ Anterior chamber paracentesis for rapid pressure relief if medical therapy is insufficient.
- ⑤ Once cornea clears: laser peripheral iridotomy (LPI) — the definitive treatment — typically bilaterally given the high fellow-eye risk.
- ⑥ If LPI is not feasible: surgical iridectomy or lensectomy, particularly when a phacomorphic component is present.
Treatment
- First-line medical: topical timolol 0.5%, a topical alpha agonist (e.g., brimonidine), a topical and/or oral carbonic anhydrase inhibitor (e.g., acetazolamide), with pilocarpine 2–4% added once IOP is lower.
- IV mannitol reserved for refractory, severe IOP elevation.
- Definitive treatment: laser peripheral iridotomy; surgical iridectomy or cataract extraction (lensectomy) when LPI is not feasible or a phacomorphic component persists.
Follow-up
- Recheck IOP within hours of starting treatment to judge response.
- Clinic visit 1–2 days later for LPI if not performed acutely.
- After LPI: confirm IOP is controlled, then transition to routine follow-up; evaluate the fellow eye for prophylactic LPI.
- Long term: monitor for chronic angle-closure glaucoma from residual synechial angle closure.
Clinical Pearl
💡 Clinical Pearl
Pilocarpine can fail as a first-line agent at very high IOP because the ischaemic iris sphincter cannot respond to cholinergic stimulation — other IOP-lowering agents should be used first to allow the sphincter to recover before adding pilocarpine.
Differential Diagnoses
| Condition | Key Distinguishing Point |
|---|---|
| Acute conjunctivitis | Discharge/itching without severe pain, normal cornea, normal pupil and IOP. |
| Anterior uveitis | Ciliary flush and pain, but IOP usually normal or low; cells/flare present; pupil often miotic, not mid-dilated. |
| Migraine with aura | No red eye, no elevated IOP; transient visual phenomena resolving over minutes. |
| Corneal abrasion/keratitis | History of trauma or lens wear, fluorescein-positive epithelial defect, normal IOP. |
| Orbital cellulitis | Proptosis, pain with eye movement, fever; IOP typically not markedly elevated by the same mechanism. |