Acute Angle Closure Glaucoma
Summary
Acute Angle Closure Glaucoma (AACG) is an ophthalmic emergency caused by rapid obstruction of aqueous humour drainage leading to a precipitous rise in intraocular pressure (IOP), typically greater than 40-60 mmHg. The closure of the anterior chamber angle by the peripheral iris blocks access to the trabecular meshwork. Patients present with severe unilateral eye pain, headache, nausea/vomiting, and visual disturbance (haloes around lights, reduced acuity). Classical examination findings include a red eye with ciliary flush, hazy cornea (oedema), fixed mid-dilated pupil, and a "stony hard" eye on palpation. Immediate treatment with intravenous acetazolamide, topical pressure-lowering agents, and pilocarpine is required to prevent permanent optic nerve damage. Definitive treatment is laser peripheral iridotomy (LPI) to both eyes (the fellow eye is at high risk).
Key Facts
- Definition: Acute obstruction of aqueous outflow due to iris apposition to trabecular meshwork
- Emergency: Vision-threatening; untreated can cause permanent blindness within hours
- IOP: Typically greater than 40 mmHg (can exceed 60 mmHg)
- Classic triad: Eye pain + reduced vision + nausea/vomiting
- Diagnostic finding: Fixed, mid-dilated pupil
- Risk factors: Hypermetropia (long-sighted), Asian ethnicity, female sex, age greater than 60
- Immediate treatment: IV acetazolamide 500mg + topical pilocarpine + timolol + position supine
Clinical Pearls
"Vomiting + Red Eye = Think AACG": Severe AACG causes intense vagal stimulation leading to nausea and vomiting. A patient with red eye and vomiting should NOT be diagnosed with gastroenteritis or migraine.
The Mid-Dilated Pupil: Unlike other causes of red eye, AACG causes a fixed, mid-dilated pupil (4-6mm) that does not react to light. This is virtually pathognomonic.
Treat the Fellow Eye: The fellow eye has the same anatomical predisposition and is at very high risk of AACG. Prophylactic laser iridotomy is always performed on both eyes.
Why This Matters Clinically
AACG can cause permanent visual loss within hours if untreated. It is frequently misdiagnosed as migraine, sinusitis, or gastroenteritis because of headache and vomiting. A high index of suspicion and recognising the cardinal signs (red eye, fixed mid-dilated pupil, hazy cornea) is essential for emergency physicians and generalists.
Incidence & Prevalence
- Incidence of AACG: 12-100 per 100,000 per year (varies by ethnicity)
- Prevalence of primary angle closure: 0.5-10% (highest in Asian populations)
- Peak age: Greater than 60 years
- Trend: Increasing with ageing population
Demographics
| Factor | Details |
|---|---|
| Age | Increases sharply after 40; peak greater than 60 |
| Sex | Female:Male 3-4:1 |
| Ethnicity | Highest in Asian (especially Chinese, Vietnamese), Inuit; lower in Caucasians, Africans |
| Geography | Southeast Asia, Mongolia have highest rates |
Risk Factors
Non-Modifiable:
- Female sex
- Age greater than 60
- Asian or Inuit ethnicity
- Hypermetropia (long-sightedness) — smaller eyes, shallower anterior chamber
- Positive family history
- Nanophthalmos (very small eye)
Modifiable:
| Risk Factor | Mechanism/Association |
|---|---|
| Dim lighting | Pupil dilation (mydriasis) precipitates attack |
| Medications | Anticholinergics, sympathomimetics, topical mydriatics |
| Stress, anxiety | May precipitate attack |
| Prone position | Lens moves forward |
Mechanism
Step 1: Anatomical Predisposition
- Shallow anterior chamber (hypermetropic, small eyes)
- Narrow angle between iris and cornea
- Short axial length; thick, anteriorly positioned lens
Step 2: Pupillary Block
- Aqueous humour is produced by ciliary body (posterior chamber)
- Normally flows through pupil to anterior chamber, then drains via trabecular meshwork
- When iris contacts lens, aqueous cannot flow through pupil ("pupillary block")
- Pressure builds in posterior chamber, pushing iris forward
Step 3: Angle Closure
- Peripheral iris pushed against trabecular meshwork
- Drainage angle completely blocked
- Aqueous cannot escape
Step 4: Acute IOP Rise
- Rapid accumulation of aqueous
- IOP rises from 10-20 mmHg to 40-80+ mmHg
- Causes corneal oedema (hazy cornea), optic nerve ischaemia
- Symptoms: severe pain, visual loss, nausea/vomiting (vagal response)
Classification
| Type | Features |
|---|---|
| Primary Angle Closure Suspect | Narrow angle on gonioscopy; no elevated IOP or damage |
| Primary Angle Closure | Closed angle + elevated IOP or peripheral anterior synechiae |
| Primary Angle Closure Glaucoma | Angle closure + glaucomatous optic neuropathy |
| Acute Angle Closure Crisis | Acute attack with symptoms; IOP usually greater than 40 |
Anatomical Considerations
- Anterior chamber depth less than 2-3mm increases risk
- Lens thickens with age, pushing iris forward
- Plateau iris: Iris root insertion is forward, not from pupillary block
Symptoms
Classic Presentation:
Associated Symptoms:
Atypical Presentations:
Signs
Affected Eye:
Fellow Eye:
Red Flags
[!CAUTION] Red Flags — Immediate action required if:
- Eye pain with fixed, mid-dilated pupil
- Sudden visual loss with red eye
- "Stony hard" eye on palpation
- Nausea/vomiting with headache and red eye
- Haloes around lights with reduced vision
- IOP greater than 40 mmHg on measurement
Structured Approach
General:
- Appears distressed, pale, or vomiting
- May be mistaken for systemic illness
Eye Examination:
- Visual acuity: Reduced (may be counting fingers or worse)
- External: Red eye with ciliary flush
- Cornea: Hazy, oedematous (steamy)
- Pupil: Fixed, mid-dilated (4-6mm), irregular or oval, unreactive
- Anterior chamber: Shallow (assess with torch from side — shadow on nasal iris)
- IOP: Very elevated (can be estimated by palpation — "stony hard")
- Fundoscopy: May be difficult due to corneal haze; look for cupping
Comparison with Fellow Eye:
- Fellow eye usually appears normal
- Check for narrow angles (shallow anterior chamber)
Special Tests
| Test | Technique | Positive Finding | Clinical Significance |
|---|---|---|---|
| IOP measurement | Tonometry (Goldmann, iCare) | Greater than 40 mmHg | Confirms diagnosis |
| Pupil assessment | Shine light; observe reaction | Fixed, mid-dilated | Pathognomonic |
| "Flashlight test" | Shine torch from temporally | Shadow on nasal iris | Shallow anterior chamber |
| Gonioscopy | Specialist; visualise angle | Closed angle; no trabecular meshwork visible | Confirms mechanism (specialist) |
| Slit-lamp biomicroscopy | Specialist examination | Corneal oedema, shallow AC | Detailed assessment |
First-Line (Bedside)
- Visual acuity — Document baseline (often significantly reduced)
- Tonometry — IOP measurement; greater than 40 mmHg diagnostic
- Direct ophthalmoscopy — May be difficult due to corneal haze; assess optic disc
Laboratory Tests
| Test | Expected Finding | Purpose |
|---|---|---|
| Usually none required | - | Diagnosis is clinical |
| U&Es | Baseline | If IV mannitol planned (osmotic diuretic) |
| Glucose | Baseline | Rule out diabetes-related complications |
Imaging
| Modality | Findings | Indication |
|---|---|---|
| Anterior segment OCT | Narrow or closed angle; iris-cornea apposition | Confirm angle anatomy; specialist |
| Ultrasound biomicroscopy | Closed angle; plateau iris | Specialist evaluation |
| B-scan ultrasound | Rule out posterior segment pathology | If view obscured |
Diagnostic Criteria
Clinical Diagnosis Based on:
- Acute onset of symptoms (pain, reduced vision, nausea/vomiting)
- Signs: Red eye, hazy cornea, fixed mid-dilated pupil
- Elevated IOP (greater than 40 mmHg, often greater than 60 mmHg)
- Gonioscopy showing closed angle (specialist confirmation)
Management Algorithm
Immediate Treatment (Emergency)
Positioning:
- Lie patient SUPINE — allows lens to fall backward, may open angle
Medical Therapy:
| Drug | Dose/Route | Mechanism |
|---|---|---|
| Acetazolamide | 500mg IV stat (or 250mg IV + 250mg PO) | Carbonic anhydrase inhibitor — reduces aqueous production |
| Timolol 0.5% | 1 drop topically | Beta-blocker — reduces aqueous production |
| Brimonidine 0.2% | 1 drop topically | Alpha-2 agonist — reduces aqueous production |
| Pilocarpine 2% | 1 drop every 15 min × 4 doses | Miotic — constricts pupil, opens angle |
| Prednisolone 1% | 1 drop topically | Reduces inflammation (after pressure control) |
If IOP Not Responding:
- IV Mannitol 1-2 g/kg over 45-60 min (osmotic diuretic — reduces vitreous volume)
- Requires cardiac monitoring; avoid in heart failure
Symptom Control:
- Antiemetic: Ondansetron 4mg IV or cyclizine 50mg IV
- Analgesia: Paracetamol IV; opioids if severe
Definitive Treatment
Laser Peripheral Iridotomy (LPI):
- Creates a hole in the peripheral iris
- Allows aqueous to bypass the pupillary block
- Performed once IOP controlled (usually within 24-48 hours)
- Must be performed on BOTH eyes — fellow eye at very high risk
Surgical Iridectomy:
- If laser iridotomy not possible (corneal oedema, patient factors)
- Surgical creation of iris opening
Post-attack Management:
- Long-term topical IOP-lowering drops may be required
- Monitor for chronic angle closure or glaucomatous damage
Disposition
- Emergency ophthalmology referral: Same-day; all suspected AACG
- Admission: If IOP uncontrolled, severe, or needing IV mannitol
- Follow-up: Within 24-48 hours for LPI; long-term monitoring for glaucoma
Immediate (Hours)
| Complication | Incidence | Presentation | Management |
|---|---|---|---|
| Permanent vision loss | 10-20% if delayed | No visual improvement | Prevention by early treatment |
| Optic nerve ischaemia | Can occur within hours | Cupped pale disc | IOP reduction |
| Corneal decompensation | Variable | Persistent haze | Corneal care; may need graft |
Early (Days-Weeks)
- Persistent elevated IOP: May require ongoing medication or surgery
- Peripheral anterior synechiae: Scarring of angle; chronic angle closure
- Cataract: Worsened by attack or pilocarpine use
Late (Months-Years)
- Chronic angle closure glaucoma: Progressive optic neuropathy
- Fellow eye attack: 50-75% risk if LPI not performed
- Recurrent attacks: If LPI fails or additional mechanisms (plateau iris)
Natural History
- Untreated: Can cause complete, permanent visual loss within hours to days
- With treatment: Excellent visual outcomes if treated promptly
- Fellow eye will often develop AACG without prophylactic LPI
Outcomes with Treatment
| Variable | Outcome |
|---|---|
| Visual recovery if treated within hours | 80-90% good outcome |
| Permanent visual loss if delayed | 10-30% |
| Success of LPI | Greater than 90% |
| Fellow eye risk without prophylactic LPI | 50-75% over 5-10 years |
| Need for ongoing IOP-lowering therapy | 30-50% |
Prognostic Factors
Good Prognosis:
- Rapid recognition and treatment
- IOP lowered within 2-4 hours
- Successful LPI to both eyes
- No pre-existing glaucomatous damage
Poor Prognosis:
- Delayed presentation (greater than 24 hours)
- Very high IOP (greater than 60 mmHg)
- Pre-existing optic nerve damage
- Failed LPI requiring surgery
Key Guidelines
- Royal College of Ophthalmologists Guidelines — Glaucoma management. RCOphth
- NICE Glaucoma Guideline (NG81) — Diagnosis and management of chronic open-angle glaucoma and ocular hypertension. (Angle closure addressed in clinical practice). NICE
- European Glaucoma Society (EGS) Guidelines — Terminology and guidelines for glaucoma (5th edition). EGS
- American Academy of Ophthalmology PPP — Primary angle closure. AAO
Landmark Trials
EAGLE Study (Azuara-Blanco et al. 2016) — Clear lens extraction vs LPI
- 419 patients with primary angle closure
- Key finding: Clear lens extraction more effective than LPI for IOP control in patients over 50
- Clinical Impact: Raised consideration of early lens extraction as definitive treatment
He et al. (2006) — Prevalence of angle closure in Asia
- Population-based study in Mongolia
- Key finding: Angle closure is the predominant form of glaucoma in East Asian populations
- Clinical Impact: Highlighted ethnic variation in glaucoma type
Evidence Strength
| Intervention | Level | Key Evidence |
|---|---|---|
| IV Acetazolamide | 4 | Expert consensus |
| Topical IOP-lowering agents | 4 | Expert consensus |
| Pilocarpine | 4 | Longstanding practice |
| Laser Peripheral Iridotomy | 1b | RCTs (EAGLE) |
| Prophylactic LPI to fellow eye | 2a | Observational studies |
What is Acute Angle Closure Glaucoma?
Acute angle closure glaucoma is a sudden and serious eye condition where the pressure inside your eye rises very quickly. This happens when the drainage system inside your eye becomes blocked. It is an emergency because if not treated quickly, it can cause permanent blindness.
Why does it happen?
Inside your eye, a fluid called aqueous humour is constantly being made and drained away. In angle closure glaucoma, the drain (at the angle where the coloured part of the eye meets the clear front part) gets blocked by the iris. The fluid builds up, and the pressure rises rapidly.
You are more at risk if you are:
- Over 60 years old
- Long-sighted (hypermetropic)
- Female
- Of Asian or Inuit ethnicity
- Related to someone who has had this condition
What are the symptoms?
- Severe pain in one eye
- Blurred vision
- Seeing rainbow-coloured haloes around lights
- Headache (often on the same side as the affected eye)
- Nausea and vomiting
- The eye looks red
How is it treated?
- Emergency treatment: Medicines are given immediately to lower the eye pressure — including drops and an injection. You may be asked to lie flat.
- Laser treatment (iridotomy): Once the pressure is controlled, a laser is used to create a tiny hole in the iris to help fluid drain properly. This is done on BOTH eyes because the other eye is also at risk.
- Follow-up: You will need regular check-ups to make sure the pressure stays normal and your optic nerve is healthy.
What to expect
- With prompt treatment, most people regain good vision
- The laser treatment usually prevents future attacks
- Some people may need long-term eye drops
- The other eye will also be treated to prevent an attack
When to seek help
Go immediately to A&E or call 999 if you have:
- Sudden, severe eye pain
- Blurred vision with a red eye
- Seeing haloes around lights
- Nausea or vomiting with eye symptoms
- A fixed, dilated pupil
Primary Guidelines
- European Glaucoma Society. Terminology and Guidelines for Glaucoma (5th Edition). 2020. EGS
- National Institute for Health and Care Excellence. Glaucoma: diagnosis and management (NG81). 2017. NICE
Key Trials
- Azuara-Blanco A, et al. Effectiveness of early lens extraction for the treatment of primary angle-closure glaucoma (EAGLE): a randomised controlled trial. Lancet. 2016;388(10052):1389-1397. PMID: 27707498
- He M, et al. The rate of visual field progression in primary angle-closure glaucoma. Ophthalmology. 2006;113(8):1266-1272. PMID: 16762436
- Lam DS, et al. Current approaches to the management of angle-closure glaucoma. Arch Ophthalmol. 2002;120(10):1314-1321. PMID: 12365909
Further Resources
- Royal College of Ophthalmologists: rcophth.ac.uk
- Glaucoma UK: glaucoma.uk
- NHS Glaucoma: nhs.uk/conditions/glaucoma
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Acute angle closure glaucoma is an ophthalmic emergency. If you have sudden eye pain with visual symptoms, seek immediate medical attention.