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acute angle-closure glaucoma

ophthalmic emergency caused by sudden obstruction of aqueous outflow — painful red eye with fixed mid-dilated pupil and raised intraocular pressure

ophthalmologyless-commonacute

About This Page

This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.

The Bottom Line

  • Ophthalmic EMERGENCY — risk of permanent vision loss within hours
  • Classic presentation: severe eye pain, red eye, haloes around lights, reduced visual acuity, nausea/vomiting
  • Key sign: fixed mid-dilated pupil, hazy cornea (oedema), IOP >40 mmHg
  • Immediate treatment: pilocarpine 4% (constricts pupil, opens drainage angle) + IV acetazolamide 500 mg + topical beta-blocker (timolol)
  • Definitive: laser peripheral iridotomy (both eyes — fellow eye is at risk)

Overview

Acute angle-closure glaucoma occurs when the peripheral iris physically blocks the trabecular meshwork, preventing aqueous humour drainage and causing a rapid rise in intraocular pressure (IOP). This is a true ophthalmic emergency — sustained high IOP damages the optic nerve and can cause irreversible vision loss within hours. Risk factors include hypermetropia (long-sighted/small eyes with shallow anterior chambers), advancing age, female sex, Asian ethnicity, and drugs that dilate the pupil (anticholinergics, sympathomimetics).

Epidemiology

Acute angle closure accounts for approximately 10% of glaucoma cases but a disproportionate share of glaucoma-related blindness. It is more common in women (3:1), older adults, and people of East Asian descent. Hypermetropic (far-sighted) patients with anatomically narrow anterior chambers are at highest risk. Precipitants include dim lighting (pupil dilation), topical mydriatics, and systemic anticholinergics (tricyclics, antihistamines).

Clinical Features

Symptoms
Severe unilateral eye pain — often described as the worst eye pain ever experienced
Reduced visual acuity — blurred or foggy vision
Haloes around lights (corneal oedema diffracts light)
Nausea and vomiting (vagal response to pain/raised IOP) — may mimic acute abdomen
Headache (may be misdiagnosed as migraine)
Signs
Red eye — ciliary (circumcorneal) injection
Fixed MID-DILATED pupil (4–6 mm, oval, unreactive to light)
Hazy/cloudy cornea (oedema from raised IOP)
Markedly raised IOP on tonometry (>40 mmHg, often 50–80)
Hard globe on palpation (stony hard compared to fellow eye)
Shallow anterior chamber on slit-lamp examination

Investigations

First-line
TonometryIOP markedly elevated — often 50–80 mmHg (normal 10–21). Confirms diagnosis
Slit-lamp examinationShallow anterior chamber, corneal oedema, mid-dilated fixed pupil, ciliary flush
Second-line
GonioscopyVisualises the drainage angle — confirms closure. Performed once acute episode treated
Visual acuityReduced on the affected side — may be significantly decreased if optic nerve damage
Specialist
Anterior segment OCTImaging of anterior chamber angle anatomy — guides further management
Fellow eye assessmentEssential — narrow angle in the fellow eye indicates prophylactic laser iridotomy needed
1
Immediate medical management (emergency)
  • Pilocarpine 4% drops to affected eye (every 5 min for 30 min, then QDS) — constricts pupil, pulls iris from angle
  • Also apply pilocarpine 1% to fellow eye prophylactically
  • IV acetazolamide 500 mg stat (reduces aqueous production)
  • Topical beta-blocker: timolol 0.5% to affected eye (reduces aqueous production)
  • Topical steroid: dexamethasone/prednisolone (reduces inflammation)
  • Lie patient supine (gravitational effect helps open the angle)
  • Analgesia and antiemetic
2
Definitive treatment
  • Laser peripheral iridotomy (YAG laser) — creates a hole in the peripheral iris allowing aqueous bypass
  • Perform on BOTH eyes (fellow eye prophylactically — ~50% will develop acute closure within 5 years)
  • Timing: once IOP controlled and cornea cleared sufficiently for laser
3
If medical treatment fails to reduce IOP
  • Laser peripheral iridoplasty
  • Surgical iridectomy
  • Lens extraction (cataract surgery effectively deepens the anterior chamber — increasingly used as primary treatment)

Complications

  • Permanent vision loss: Optic nerve damage from sustained high IOP — the central concern
  • Chronic angle closure: If not definitively treated, may develop chronic raised IOP requiring long-term medication
  • Fellow eye acute attack: ~50% risk within 5 years without prophylactic iridotomy
  • Posterior synechiae: Iris adhesions from inflammation
UKMLA Exam Tips
  • 1Fixed MID-DILATED pupil + red eye + severe pain + haloes = acute angle closure. This is the classic exam presentation
  • 2Do NOT give atropine or tropicamide (mydriatics) — these will WORSEN the attack by further dilating the pupil
  • 3Pilocarpine (miotic) is first-line — it CONSTRICTS the pupil and opens the drainage angle
  • 4Red eye differentials: acute glaucoma (mid-dilated fixed pupil), anterior uveitis (small irregular pupil), conjunctivitis (normal pupil)
  • 5Drugs that precipitate attacks: anticholinergics (TCAs, antihistamines), sympathomimetics, topical mydriatics
  • 6Always treat the FELLOW EYE with prophylactic laser iridotomy — this is a bilateral condition
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Verified Sources & References

NICE NG81 — Glaucoma: diagnosis and management
RCOphth Guidelines