Acute angle-closure glaucoma
A sudden obstruction of aqueous outflow causes a rapidly painful rise in intraocular pressure, producing a red eye with visual symptoms and vomiting that needs same-day ophthalmology treatment.
Definition
Acute angle-closure glaucoma is a sudden symptomatic rise in intraocular pressure caused by closure of the iridocorneal drainage angle, most often from pupillary block. It is an ophthalmic emergency because sustained pressure can cause irreversible visual loss.
Epidemiology
Primary angle closure is more likely in older adults and in eyes with a shallow anterior segment, hypermetropia or a thickened lens; risk also varies with ancestry and family history. Dim light, pupil dilation and medicines with anticholinergic or sympathomimetic effects can precipitate an attack in susceptible eyes.
Pathophysiology
Aqueous flow through the pupil becomes obstructed in a crowded anterior segment. Posterior-chamber pressure bows the peripheral iris forward against the trabecular meshwork, closing the angle. Pressure rises rapidly, producing corneal oedema, pain, visual disturbance, iris-sphincter ischaemia and potentially optic-nerve or retinal injury. Secondary mechanisms require different treatment.
First principles
Pupillary block is an aqueous-flow problem
In a crowded, shallow anterior segment, the iris can obstruct aqueous movement through the pupil and bow forward against the trabecular meshwork. The drainage angle closes, aqueous continues to be produced and intraocular pressure rises rapidly. Older age, a thickened lens, hypermetropia and a short crowded eye increase anatomical susceptibility.1,2
The pressure spike explains the classic red-eye syndrome
High pressure causes corneal oedema and blurred vision with haloes, stimulates ocular pain pathways and may trigger nausea and vomiting. The iris sphincter becomes ischaemic, producing a fixed mid-dilated pupil. Sustained pressure compromises the optic nerve and retinal perfusion, so visual loss can become irreversible.1,2
The fellow eye is anatomically at risk
The predisposing anatomy is usually bilateral even when the attack is unilateral. After the acute eye is stabilised, ophthalmology assesses the fellow eye and plans preventive treatment according to the angle, mechanism and risk factors rather than discharging it as normal.3,1
Not every angle-closure picture is pupillary block
Secondary angle closure can result from inflammation, lens-related mechanisms, neovascularisation, medication effects or posterior pressure. The definitive intervention must match the mechanism; an emergency red eye should not be reduced to a routine primary pupillary-block pathway without ophthalmic assessment.1,2
Presentation
Sudden severe unilateral eye pain with headache, blurred vision or haloes, a red eye, hazy cornea and a fixed mid-dilated pupil, often accompanied by nausea or vomiting.1,2
Cardinal features
- Severe ocular pain with headache
- Blurred vision and haloes around lights
- Red eye with circumcorneal injection
- Hazy or oedematous cornea
- Fixed, mid-dilated or oval pupil with poor light reaction
- Nausea or vomiting
Red flags
- Rapid visual loss or a markedly raised intraocular pressure
- Severe pain with a cloudy cornea and fixed pupil
- Failure of pressure to fall with initial emergency treatment
- Bilateral or fellow-eye angle-closure risk
- Atypical features suggesting a secondary mechanism
- Systemic deterioration or vomiting that obscures the eye presentation
Investigations
Visual acuity and urgent intraocular-pressure measurement
Record visual acuity and measure IOP urgently with appropriate ophthalmic equipment. Pressure confirms the emergency and provides a response marker, but referral must not be delayed while trying to obtain a non-specialist measurement.
Expected finding: Markedly raised IOP with reduced visual acuity in the affected eye.
1,4,2Slit-lamp anterior-segment examination
Assess the cornea, anterior chamber depth, iris, pupil, inflammation and ciliary injection, and look for signs suggesting uveitis, trauma or a secondary mechanism.
Expected finding: Corneal oedema, shallow anterior chamber, fixed mid-dilated pupil and circumcorneal injection.
1,4Gonioscopy of both eyes when feasible
Gonioscopy confirms angle configuration and distinguishes occludable or closed angles from open-angle disease. It also helps ophthalmology decide whether the fellow eye needs laser or another preventive intervention.
Expected finding: Closed or occludable angle in primary angle closure; a different configuration may indicate secondary angle closure.
1,4Optic-nerve, fundus and mechanism assessment after stabilisation
Once the cornea and pressure permit examination, assess the optic nerve and retina for damage and document a baseline. Consider lens, inflammatory, neovascular, drug-induced or other secondary causes when the presentation is atypical.
Expected finding: The disc may be normal acutely or show established glaucomatous damage; mechanism-specific findings guide definitive treatment.
1,4,2Management
| Step | Detail | Source |
|---|---|---|
| Arrange same-day emergency ophthalmology assessment | Treat suspected acute angle closure as an ophthalmic emergency. Contact ophthalmology immediately and arrange same-day assessment or admission; irreversible optic-nerve damage can occur if the pressure remains high. Do not delay transfer for a complete community work-up.3,1,2 | Royal College of Ophthalmologists, Management of Angle Closure Glaucoma guideline |
| Avoid worsening the angle while transfer is arranged | Keep the patient comfortable and supine if this is the local emergency pathway while urgent transfer is organised, provide analgesia and an antiemetic as clinically appropriate, and avoid mydriatic or anticholinergic medicines unless ophthalmology specifically directs them. Do not use a routine red-eye pathway.1,2 | Royal College of Ophthalmologists angle-closure guideline and NICE CKS glaucoma |
| Start ophthalmology-led pressure-lowering therapy promptly | Under the emergency ophthalmology protocol, lower aqueous production and pressure using appropriate topical agents such as a beta-blocker and alpha-agonist, systemic or oral acetazolamide when suitable, and a hyperosmotic agent if pressure remains uncontrolled. Check contraindications, interactions, renal function and cardiovascular status and use current BNF and local ophthalmology doses.1,5,6 | Royal College of Ophthalmologists angle-closure guideline and BNF acetazolamide/apraclonidine |
| Use pilocarpine only once the sphincter can respond | Pilocarpine may be added to constrict the pupil and open the angle after pressure has started to fall. Do not rely on pilocarpine while IOP is above 40 mmHg because an ischaemic iris sphincter may not respond; follow the ophthalmology protocol and current BNF. Treat inflammation when indicated by the ophthalmologist.1,7 | Royal College of Ophthalmologists angle-closure guideline and BNF pilocarpine |
| Perform definitive laser or surgical treatment | Once the cornea is sufficiently clear and pressure is controlled, perform laser peripheral iridotomy or another mechanism-appropriate definitive intervention in the affected eye. If laser is not possible or the lens is a major contributor, ophthalmology may consider iridoplasty, lens extraction or another surgical option.1,3 | Royal College of Ophthalmologists, Management of Angle Closure Glaucoma guideline |
| Protect the fellow eye and identify secondary mechanisms | Assess the fellow eye urgently and provide prophylactic treatment when indicated, commonly laser peripheral iridotomy for a comparable primary pupillary-block risk. If the mechanism is secondary, treat the cause and do not assume that an iridotomy alone resolves the risk.1,3,2 | Royal College of Ophthalmologists angle-closure guideline |
| Reassess pressure, vision and optic-nerve risk after the attack | Continue ophthalmology follow-up with IOP, visual acuity, gonioscopy, optic-nerve assessment and visual-field testing when the eye is able to participate. Review adherence, medication triggers and the need for further laser, lens or glaucoma treatment; safety-net recurrent pain, halos or visual change as an emergency.1,4,2 | Royal College of Ophthalmologists angle-closure guideline and NICE NG81 |
Illustrations
Differentials
Anterior uveitis
Pain and photophobia with a small or irregular pupil, cells or flare and a different pressure pattern.
Acute conjunctivitis
Discharge and diffuse redness with preserved vision, a reactive pupil and no pressure emergency.
Scleritis
Deep severe ocular pain with scleral injection but no typical fixed mid-dilated pupil or pressure spike.
Acute corneal disease
Pain and photophobia with epithelial or stromal corneal findings but no angle-closure syndrome.
Secondary angle closure
Inflammatory, lens-related, neovascular, drug-induced or posterior-pressure mechanism requiring cause-specific treatment.
Complications
- Permanent optic-nerve damage and visual-field loss
- Chronic angle-closure glaucoma and peripheral anterior synechiae
- Corneal oedema and decompensation
- Cataract or lens-related contribution
- Recurrent attack or fellow-eye attack without preventive treatment
Prognosis
Prompt pressure reduction and definitive mechanism-specific treatment can preserve vision, but delay risks permanent optic-nerve injury. The fellow eye requires urgent specialist risk assessment because the predisposing anatomy is often bilateral.
Guidelines
- Management of Angle Closure Glaucoma (Royal College of Ophthalmologists, 2022)
- Glaucoma: diagnosis and management (NG81) (NICE, 2022)
References
- Royal College of Ophthalmologists, The Management of Angle-Closure Glaucoma full guideline (Clinical guideline, June 2022)Published 24 Jun 2022
- NICE CKS, Glaucoma
- Royal College of Ophthalmologists, Management of Angle Closure Glaucoma guideline recommendations (Clinical guideline, 24 June 2022)Published 24 Jun 2022
- NICE, Glaucoma: diagnosis and management (NG81)Published 1 Nov 2017 | Updated 26 Jan 2022
- BNF, Acetazolamide
- BNF, Apraclonidine
- BNF, Pilocarpine
- BNF, Timolol maleate
Evidence checked: 2026-08-03
This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.