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Ophthalmology
Emergency Medicine
EMERGENCY

Acute Angle-Closure Glaucoma

High EvidenceUpdated: 2024-12-21

On This Page

Red Flags

  • Severe eye pain
  • Red eye with fixed mid-dilated pupil
  • Severely reduced vision
  • Haloes around lights
  • Nausea and vomiting
  • Rock-hard eye on palpation
Overview

Acute Angle-Closure Glaucoma

1. Clinical Overview

Summary

Acute angle-closure glaucoma (AACG) is an ophthalmic emergency caused by sudden obstruction of aqueous outflow due to iridotrabecular apposition. This causes rapid rise in intraocular pressure (IOP), typically over 40 mmHg. Classic presentation is severe eye pain, red eye, fixed mid-dilated pupil, reduced vision, and haloes around lights. Nausea and vomiting are common. Untreated, it causes irreversible optic nerve damage within hours. Treatment is urgent IOP reduction and definitive laser peripheral iridotomy.

Key Facts

  • Mechanism: Iris blocks trabecular meshwork → aqueous can't drain → IOP rises rapidly
  • IOP: Often over 40 mmHg (normal 10-21)
  • Presentation: Severe eye pain, red eye, mid-dilated fixed pupil, reduced vision, haloes
  • Emergency: Can cause permanent blindness within hours
  • Treatment: Medical IOP reduction → laser peripheral iridotomy (definitive)

Clinical Pearls

Mid-dilated FIXED pupil = AACG until proven otherwise

Patient may present to A&E with "headache and vomiting" — always check the eyes

Precipitants: Dim lighting, mydriatic drugs, anticholinergics

Why This Matters Clinically

AACG is a true ophthalmic emergency. Delayed treatment leads to permanent vision loss. Non-ophthalmologists must recognise it to ensure urgent referral.


2. Epidemiology

Incidence

  • 0.1-0.2% lifetime risk
  • More common in Asians (shallower anterior chamber)
  • Peak age: 55-70 years

Demographics

  • Female predominance (3:1)
  • Hyperopia (long-sighted) — shallow anterior chamber
  • Asian ethnicity

Risk Factors

FactorNotes
HyperopiaShallow anterior chamber
Asian ethnicityAnatomical predisposition
Female sex
Family history
Increasing ageLens thickens
Dim lightingPupil dilates
Mydriatic drugsTropicamide, atropine
AnticholinergicsMany medications

3. Pathophysiology

Mechanism

  1. Anatomically narrow angle (shallow anterior chamber)
  2. Pupil dilates (dim light, drugs)
  3. Iris bows forward (pupil block)
  4. Iris occludes trabecular meshwork
  5. Aqueous humour cannot drain
  6. Rapid IOP rise

Why Damage Occurs

  • High IOP compresses optic nerve fibres
  • Ischaemia to optic nerve
  • Permanent ganglion cell death within hours

Pupil Block

  • Most common mechanism
  • Aqueous trapped behind iris → iris bows forward
  • Relieved by iridotomy

4. Clinical Presentation

Symptoms

Signs

Red Flags

FindingSignificance
Fixed mid-dilated pupilClassic AACG
Rock-hard eyeVery high IOP
Cloudy corneaCorneal oedema from high IOP
Profound vision lossEmergency

Severe eye pain — unilateral
Common presentation.
Reduced vision — often profound
Common presentation.
Haloes around lights — corneal oedema
Common presentation.
Headache — may be frontal or periorbital
Common presentation.
Nausea and vomiting — vagal response to pain
Common presentation.
5. Clinical Examination

Visual Acuity

  • Often severely reduced (counting fingers or worse)

Pupil

  • Mid-dilated (4-6 mm)
  • Fixed (poorly reactive or non-reactive)
  • Oval shape

Anterior Segment

  • Ciliary injection (red eye)
  • Corneal oedema (hazy)
  • Shallow anterior chamber

Palpation

  • Affected eye feels hard compared to other eye

IOP Measurement

  • Tonometry: Often over 40 mmHg (can be 60-80+)

Gonioscopy

  • Closed angle (no trabecular meshwork visible)

6. Investigations

Clinical Diagnosis

  • Primarily clinical — classic features

Tonometry

  • IOP measurement essential
  • Often over 40 mmHg

Slit Lamp

  • Corneal oedema
  • Shallow anterior chamber
  • Cells/flare

Gonioscopy

  • Confirms closed angle

Imaging

  • Anterior segment OCT (if available)

Classification & Staging

By Mechanism

TypeMechanism
Pupil blockMost common; aqueous trapped behind iris
Plateau irisCiliary body pushes iris forward
PhacomorphicSwollen cataractous lens
NeovascularNew vessels in angle

By Duration

  • Acute (sudden onset)
  • Subacute (recurrent, self-limiting attacks)
  • Chronic (gradual angle closure)

7. Management

Immediate — Reduce IOP

Position:

  • Supine (allows lens to fall back)

Topical Medications:

AgentClassEffect
Pilocarpine 2-4%MioticConstricts pupil, opens angle
Timolol 0.5%Beta-blockerReduces aqueous production
Apraclonidine 1%Alpha-agonistReduces aqueous production
LatanoprostProstaglandinIncreases uveoscleral outflow

Systemic Medications:

AgentEffect
IV acetazolamide 500mgCarbonic anhydrase inhibitor; reduces aqueous
IV mannitol 20%Osmotic diuretic; reduces vitreous volume

Note: Pilocarpine may not work if IOP very high (iris sphincter ischaemic)

Definitive Treatment — Laser Peripheral Iridotomy (LPI)

  • Creates hole in peripheral iris
  • Relieves pupil block
  • Allows aqueous to drain
  • Both eyes treated (fellow eye prophylaxis)

If Laser Not Possible

  • Surgical peripheral iridectomy
  • Lens extraction (if lens contributing)

Analgesia and Antiemetics

  • IV morphine, ondansetron as needed

Refer Urgently to Ophthalmology

  • Same-day assessment essential

8. Complications

Of AACG

  • Permanent vision loss
  • Optic nerve damage
  • Corneal decompensation
  • Cataract
  • Synechiae (iris adhesions)

Of Treatment

  • LPI: Glare, blurred vision (usually minor)
  • Systemic medications: Electrolyte disturbance, paraesthesia

9. Prognosis & Outcomes

Prognosis

  • Good if treated within hours
  • Permanent damage if delayed over 24-48 hours

Vision Outcome

  • Depends on duration and peak IOP
  • Some recovery possible with prompt treatment

Fellow Eye

  • High risk — prophylactic LPI indicated

10. Evidence & Guidelines

Key Guidelines

  1. Royal College of Ophthalmologists Guidelines
  2. AAO Preferred Practice Pattern: Primary Angle Closure

Key Evidence

  • Laser peripheral iridotomy is definitive treatment
  • Prophylactic iridotomy prevents attacks in fellow eye

11. Patient/Layperson Explanation

What is Acute Glaucoma?

Acute glaucoma happens when the fluid in your eye can't drain properly, causing the pressure inside the eye to rise suddenly. This is an emergency.

Symptoms

  • Severe pain in one eye
  • Red eye
  • Blurred vision
  • Seeing haloes around lights
  • Feeling sick or vomiting

What Should I Do?

  • Go to A&E immediately
  • This needs urgent treatment to save your sight

Treatment

  • Eye drops and tablets to lower the pressure
  • Laser treatment to make a small hole in the iris to help fluid drain

Resources

  • Glaucoma UK
  • NHS Glaucoma

12. References

Primary Guidelines

  1. AAO. Primary Angle Closure Disease Preferred Practice Pattern. 2020.
  2. Royal College of Ophthalmologists. Guidelines for the Management of Angle Closure. 2018.

Key Reviews

  1. Wright C, et al. Primary angle closure glaucoma: an update. Acta Ophthalmol. 2016;94(3):217-225. PMID: 26303815
  2. Prum BE Jr, et al. Primary Angle Closure Preferred Practice Pattern Guidelines. Ophthalmology. 2016;123(1):P1-P40. PMID: 26581557

Last updated: 2024-12-21

At a Glance

EvidenceHigh
Last Updated2024-12-21
Emergency Protocol

Red Flags

  • Severe eye pain
  • Red eye with fixed mid-dilated pupil
  • Severely reduced vision
  • Haloes around lights
  • Nausea and vomiting
  • Rock-hard eye on palpation

Clinical Pearls

  • Mid-dilated FIXED pupil = AACG until proven otherwise
  • Patient may present to A&E with "headache and vomiting" — always check the eyes
  • Precipitants: Dim lighting, mydriatic drugs, anticholinergics

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines