Acute angle-closure glaucoma

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Acute angle closure occurs when access to the trabecular drainage pathway becomes obstructed, causing a rapid rise in intraocular pressure. The clinical emergency is sometimes called acute angle-closure glaucoma even when permanent optic nerve damage has not yet been established. This distinction matters for accurate diagnosis, but it must not slow treatment of a symptomatic pressure crisis.

A familiar presentation is an older long-sighted person with unilateral ocular pain, coloured haloes, blurred vision and vomiting. The spectrum is wider: intermittent attacks can settle before examination, and drug-related or postoperative secondary closure can occur in younger people or both eyes simultaneously. The central decision is to identify the mechanism, reduce pressure safely and arrange an anatomical treatment where appropriate. Merely prescribing chronic glaucoma drops and sending the person home leaves the obstruction and risk unresolved.

Key points

Treat the acute symptomatic pressure rise as an emergency even before established glaucomatous optic nerve damage can be demonstrated.
Record visual acuity, pupils, pressure and anterior chamber depth in both eyes, while arranging urgent ophthalmic review.
Ask explicitly about topiramate, recent eye surgery and cataract: some secondary mechanisms worsen with pilocarpine.
Confirmed pupil-block closure needs prompt pressure reduction followed by laser peripheral iridotomy as soon as technically feasible.
The RCOphth acute pathway selects intravenous acetazolamide 250 mg once when pressure exceeds 40 mmHg, with reassessment at 30–60 minutes and further treatment directed by ophthalmology.
For pupil block, pilocarpine 2% is deferred while pressure exceeds 40 mmHg; intensive repeated instillation is discouraged.
Assess and protect the fellow eye; successful reduction of pain and pressure does not remove its risk or complete definitive care.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Crowded anterior segment

An anatomically shallow anterior chamber and increasing lens volume can bring the iris into contact with the drainage angle. Pupil dilation may precipitate obstruction in a susceptible eye.

Secondary displacement

An enlarged or displaced lens, postoperative aqueous misdirection or a drug-related supraciliary effusion can push the iris–lens diaphragm forwards, closing the angle through mechanisms that differ from relative pupil block.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Relative pupil block
Resistance to aqueous passage between lens and iris raises posterior chamber pressure relative to the anterior chamber. The peripheral iris bows forwards and obstructs access to the trabecular meshwork.
2
Pressure and corneal oedema
Rapid outflow obstruction elevates pressure, disturbs corneal endothelial function and causes stromal oedema. The resulting haze and epithelial disturbance contribute to blurred vision, haloes and examination difficulty.
3
Iris and nerve ischaemia
Severely raised pressure compromises tissue perfusion and can impair iris sphincter function. Sustained or recurrent attacks threaten the optic nerve and may leave permanent adhesions within the drainage angle.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

A painful pressure crisis

Severe eye pain, reduced vision, haloes, nausea and vomiting with a red eye should trigger emergency ophthalmic contact rather than routine glaucoma referral.

Anterior segment clues

Corneal oedema, a shallow chamber and a mid-dilated poorly reactive pupil support the diagnosis, although not every sign is present in every mechanism.

Atypical or bilateral closure

A new myopic shift, bilateral symptoms or recent topiramate initiation suggests a supraciliary effusion mechanism and changes the choice of pupil-active treatment.

Lens and postoperative clues

A markedly different central chamber depth between eyes, an intumescent cataract or recent surgery raises concern for lenticular or retrolenticular obstruction.

Red flags requiring action

Abrupt ocular pain and visual deterioration with vomiting or a hazy cornea require emergency eye assessment; do not manage presumed migraine or gastroenteritis without examining the eyes.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Immediate visual acuity, pupils and pressureFirst step
Why
Establish the severity and document the baseline while arranging treatment.
Interpretation and limitations
Measure each eye when possible; visual loss with high pressure needs urgent intervention, but a single pressure number does not determine the underlying mechanism.
02
Slit-lamp assessment and gonioscopy
Why
Confirm angle closure and identify inflammation, lens changes or adhesions.
Interpretation and limitations
Corneal oedema may initially limit gonioscopy; compare central and peripheral chamber depth and repeat angle examination after pressure and clarity improve.
03
Targeted medicines and surgical history
Why
Identify an avoidable precipitant or a secondary mechanism.
Interpretation and limitations
Specifically establish topiramate exposure, timing of dose changes, recent ocular procedures and relevant systemic medicines rather than asking only about eye drops.
04
Renal function, electrolytes and clinical assessment
Why
Support safe systemic pressure treatment and identify important contraindications.
Interpretation and limitations
Check kidney disease, electrolyte disturbance, acidosis, cardiopulmonary disease and allergy before selecting systemic or topical drugs; urgent specialist care must continue while results are obtained.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Anterior uveitis

Photophobia, inflammatory cells and a smaller or irregular pupil may indicate uveitis. Pressure can also rise during inflammatory disease, so a red eye and high pressure do not establish primary pupil block.

Corneal infection

A focal corneal infiltrate, epithelial defect, discharge or contact-lens history suggests microbial keratitis. Its urgent antimicrobial pathway differs from treating angle closure, and steroid treatment requires diagnostic care.

Neurological or gastrointestinal illness

Headache and vomiting can dominate the history, but reduced vision, an abnormal pupil or corneal haze directs attention to the eye. A neurological diagnosis should not substitute for ocular examination.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Immediate responseStabilise symptoms and identify the mechanismFirst stepA person presents with abrupt painful visual loss and suspected acute angle closure.

1Contact the receiving eye service immediately, document vision and pupils, and provide appropriate analgesia and antiemetic treatment during assessment.
2Confirm elevated pressure and a closed angle, checking both anterior chambers and the history for secondary lenticular, postoperative or drug-related causes.
3Select initial pressure-lowering treatment with the ophthalmologist after reviewing renal, electrolyte, respiratory, cardiac and allergy risks; arrange reassessment within the acute service.

02Confirmed pupil blockLower pressure and relieve the obstructionExamination supports acute primary closure through pupil block or associated plateau-iris anatomy.

1Use topical aqueous suppressants and systemic acetazolamide as appropriate; defer pilocarpine at very high pressure until the iris can respond.
2Reassess symptoms, pressure and corneal clarity after initial treatment; undertake peripheral iridotomy promptly when technically possible and address the contralateral eye.
3EscalationIf medical treatment fails or corneal haze prevents iridotomy, escalate to the glaucoma team for options such as iridoplasty or cyclodiode rather than continuing ineffective drops indefinitely.

03Secondary mechanismTreat the cause of forward displacementFindings suggest an enlarged lens, aqueous misdirection or drug-associated supraciliary effusion.

1Avoid reflex pilocarpine treatment and obtain urgent specialist confirmation of the anatomical mechanism before using a miotic.
2For suspected topiramate-associated disease, coordinate rapid discontinuation with the treating prescriber and institute appropriate pressure reduction and specialist cycloplegic treatment.
3Plan lens surgery or other mechanism-specific intervention when indicated, recognising that an iridotomy alone will not resolve a purely non-pupil-block effusion mechanism.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Rapid systemic reduction of aqueous production during an acute severe pressure rise.

Acetazolamide injection for the selected RCOphth acute pathway

The RCOphth acute-care diagram uses acetazolamide 250 mg intravenously once when intraocular pressure exceeds 40 mmHg; reassess at 30–60 minutes and have ophthalmology determine further dosing and the stop point.

This is a selected national pathway dose; local protocols may differ. The injection SmPC contraindicates marked kidney or liver dysfunction, low sodium or potassium, hyperchloraemic acidosis and relevant hypersensitivity including sulphonamides. Review respiratory and volume status; new severe breathlessness after administration requires urgent assessment.

Constricts the pupil to help reopen an angle obstructed by a responsive peripheral iris.

Pilocarpine 2% eye drops for a suitable pupil-block mechanism

Instil one drop into the affected eye initially when advised; the RCOphth pathway defers treatment if pressure is above 40 mmHg. Subsequent dosing is approximately every six hours until definitive treatment or specialist review.

Do not give an intensive repeated loading schedule. Avoid use for lenticular or retrolenticular closure because contraction may worsen forward displacement; specialist cycloplegia is used instead. Treatment of the fellow eye and continuation after iridotomy must be prescribed explicitly.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Permanent optic neuropathy

An inadequately treated attack can cause irreversible nerve-fibre loss and persistent visual-field damage, particularly when significant chronic angle-closure disease was already present before the acute symptoms.

Persistent angle damage

Peripheral anterior synechiae and trabecular injury may leave pressure elevated despite a patent iridotomy. Continuing glaucoma therapy and structural and functional surveillance can therefore remain necessary.

Further acute episodes

The other eye often shares the predisposing anatomy, and residual non-pupil-block crowding may persist in the treated eye. Definitive assessment of both angles is necessary after symptomatic improvement.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Acute reassessment must record pressure, corneal clarity, pain and visual function, including response after the initial 30–60-minute treatment period.
After iridotomy, verify patency and assess remaining angle closure, inflammation and pressure; a visible laser opening does not prove complete disease control.
Once the eye is comfortable and examination is reliable, establish optic nerve imaging and fields to quantify any pre-existing or attack-related damage.
Give written instructions about urgent recurrence symptoms, the fellow-eye plan, prescribed drops and the next appointment before discharge from acute care.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Symptoms may fluctuate before a crisis

Intermittent haloes or aching in dim light can precede a sustained attack; apparently normal findings after symptoms settle do not remove the need to assess susceptible anatomy.

Lens extraction has an anatomical purpose

Removing a bulky lens can deepen the anterior chamber. In angle-closure disease with cataract, surgery may address both visual impairment and the mechanism of crowding after acute stabilisation.

Mannitol requires medical supervision

A hyperosmotic infusion is a specialist option, with renal function, fluid balance and cardiac risk considered explicitly. Repeated doses should not be copied into an open-ended prescription without consultant reassessment.

Pupil dilation needs a considered indication

Routine diagnostic dilation should follow an assessment of risk in a symptomatic narrow-angle eye; conversely, cycloplegia may be the correct treatment when secondary forward displacement is the cause.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for definite optic disc cupping before treating a symptomatic acute angle-closure crisis.
02
Assuming every closed angle has pupil block and instilling pilocarpine before considering secondary displacement.
03
Attributing predominant vomiting to a gastrointestinal illness without checking visual acuity and the eyes.
04
Stopping the pathway after pressure falls while leaving definitive treatment and the fellow eye unaddressed.