Acute Angle Closure Glaucoma

1. Clinical Overview

Summary

Acute Angle Closure Glaucoma (AACG), also termed Acute Primary Angle Closure (APAC), is an ophthalmic emergency characterised by rapid obstruction of aqueous humour outflow leading to a precipitous rise in intraocular pressure (IOP), typically exceeding 40-60 mmHg. [1,2] The condition arises when the peripheral iris apposes the trabecular meshwork, mechanically blocking the drainage of aqueous humour from the anterior chamber. This results in acute elevation of IOP that can cause irreversible optic nerve damage within hours if untreated. [3]

The classical presentation includes severe unilateral eye pain of acute onset, frontal or periorbital headache, nausea and vomiting (due to intense vagal stimulation), and visual disturbance including haloes around lights and markedly reduced visual acuity. [4] The pathognomonic examination findings include a red eye with ciliary injection, hazy oedematous cornea, fixed mid-dilated pupil (4-6mm) that does not react to light, and a characteristically "rock-hard" or "stony" eye on digital palpation. [5]

AACG represents a true sight-threatening emergency requiring immediate treatment. The management algorithm involves positioning the patient supine, administering intravenous acetazolamide 500mg, applying topical pressure-lowering agents (timolol, brimonidine), topical pilocarpine 2% to constrict the pupil once IOP begins to fall, and topical corticosteroids to reduce inflammation. [6,7] Definitive treatment is laser peripheral iridotomy (LPI), which must be performed on both eyes given the high risk to the anatomically similar fellow eye. [8] Recent evidence from the EAGLE trial supports early clear lens extraction as an alternative definitive treatment in patients over 50 years. [9]

Key Facts

Clinical Pearls

"Vomiting + Red Eye = Think AACG": The intense vagal stimulation in severe AACG causes profound nausea and vomiting. A patient presenting with a red eye and vomiting should NOT be diagnosed with gastroenteritis or migraine until AACG is excluded. The systemic symptoms can dominate the presentation. [4]

The Mid-Dilated Pupil is Pathognomonic: Unlike other causes of acute red eye, AACG produces a fixed, mid-dilated pupil (4-6mm) that does not react to light. This finding, combined with a hazy cornea and rock-hard eye, is virtually diagnostic. The mid-dilation reflects iris sphincter ischaemia. [5]

Always Treat the Fellow Eye: The fellow eye shares the same anatomical predisposition (shallow anterior chamber, narrow angle) and carries a 50-75% risk of AACG over the following years if left untreated. Prophylactic laser peripheral iridotomy should be performed on BOTH eyes. [8,10]

Pilocarpine Timing is Critical: Pilocarpine is ineffective when IOP is very high (> 50-60 mmHg) because the iris sphincter muscle becomes ischaemic and paralysed. Administer pilocarpine only after IOP begins to fall with systemic treatment, or it will not work. [6]

Why This Matters Clinically

AACG is frequently misdiagnosed in emergency departments as migraine, gastroenteritis, sinusitis, or even acute abdomen due to the prominence of systemic symptoms (headache, vomiting, abdominal discomfort). [4,11] The diagnosis requires a high index of suspicion and recognition of the cardinal ocular signs. The global burden of angle-closure glaucoma is substantial, with an estimated 20 million people affected worldwide and angle closure responsible for approximately 50% of glaucoma-related blindness despite accounting for only about 26% of glaucoma cases. [12] This disproportionate visual morbidity highlights the more aggressive nature of angle-closure disease and the critical importance of prompt recognition and treatment.

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2. Epidemiology

Incidence & Prevalence

Global epidemiological data demonstrate significant ethnic and geographic variation in the prevalence of primary angle-closure glaucoma (PACG) and acute angle-closure attacks. [12,13]

Demographics

Risk Factors

Non-Modifiable Risk Factors

Modifiable/Precipitating Factors

Medications That Can Precipitate AACG

[!WARNING] High-Risk Medications in Angle-Closure Suspects:

Anticholinergics: Atropine, hyoscine, glycopyrrolate, oxybutynin, tolterodine, tricyclic antidepressants, antihistamines (diphenhydramine), antipsychotics (chlorpromazine)

Sympathomimetics: Pseudoephedrine, phenylephrine, adrenaline/epinephrine

Sulphonamide derivatives: Topiramate (unique mechanism: uveal effusion causing angle closure)

Others: Botulinum toxin (if inadvertently into iris), selective serotonin reuptake inhibitors (rare) [18,19]

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3. Pathophysiology

Aqueous Humour Dynamics

Understanding normal aqueous humour physiology is essential for comprehending the mechanism of angle-closure glaucoma.

Normal Aqueous Production and Drainage:

• Aqueous humour is produced by the ciliary body epithelium at a rate of approximately 2-3 μL/minute [20]
• Flows from posterior chamber through pupil into anterior chamber
• Drains primarily via the trabecular meshwork (conventional pathway, 80-90%) in the iridocorneal angle
• Secondary uveoscleral (unconventional) pathway accounts for 10-20% of outflow
• Normal IOP: 10-21 mmHg (mean approximately 15 mmHg) [20]

Mechanism of Angle Closure

Step 1: Anatomical Predisposition

Certain eyes are anatomically prone to angle closure due to structural features:

Step 2: Pupillary Block

The most common mechanism of angle closure (> 90% of cases):

1. Lens-iris contact zone increases with age and in predisposed eyes
2. Resistance to aqueous flow through pupil creates relative pupillary block
3. Aqueous accumulates in posterior chamber, creating pressure gradient
4. Peripheral iris bows forward (iris bombé configuration)
5. Maximum iris-lens contact occurs at mid-dilation (3-5mm pupil) — explains why dim lighting triggers attacks

Step 3: Iridotrabecular Contact

1. Forward-bowed peripheral iris apposes trabecular meshwork
2. Aqueous drainage is mechanically blocked
3. Initially appositional (reversible with treatment)
4. Prolonged contact leads to peripheral anterior synechiae (PAS) — permanent adhesions

Step 4: Acute IOP Elevation

1. With drainage blocked, aqueous accumulates rapidly
2. IOP rises from normal (10-21 mmHg) to 40-80+ mmHg within hours
3. Corneal endothelium decompensates → corneal oedema (hazy cornea) [21]
4. Optic nerve head perfusion compromised → ischaemic damage
5. Iris sphincter ischaemia → mid-dilated, unreactive pupil
6. Ciliary body stimulation + IOP → intense pain, vagal response (nausea, vomiting)

Alternative Mechanisms of Angle Closure

Plateau Iris Syndrome:

• Abnormally anterior insertion of iris root at ciliary body
• Iris bunches in angle on dilation even without pupillary block
• LPI alone may be insufficient; laser peripheral iridoplasty may be needed
• Prevalence: 20-30% of angle-closure patients [22]

Lens-Induced Mechanisms:

• Phacomorphic: Large/swollen lens pushes iris forward
• Lens subluxation: Anterior displacement closes angle
• Intumescent cataract: Lens swelling precipitates closure

Secondary Angle Closure:

• Neovascular glaucoma: Fibrovascular membrane zips angle closed
• Uveitis: Posterior synechiae cause pupillary block
• Tumours: Ciliary body mass displaces iris
• Suprachoroidal haemorrhage/effusion: Pushes lens-iris forward
• Topiramate-induced: Ciliary body oedema and rotation

Classification of Primary Angle Closure Disease

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4. Clinical Presentation

Symptoms

Cardinal Symptoms of Acute Attack

Systemic Symptoms (Often Dominant)

• Abdominal pain: Vagal-mediated; can mimic acute abdomen
• Bradycardia: Parasympathetic activation
• Diaphoresis: Autonomic response to severe pain
• Prostration: Patient appears systemically unwell

[!CAUTION] Diagnostic Pitfall: Systemic symptoms (vomiting, abdominal pain, headache) may dominate the presentation, leading to misdiagnosis as migraine, gastroenteritis, acute abdomen, or even stroke. Always examine the eyes in patients with headache and vomiting. [4,11]

Prodromal Symptoms (Subacute Attacks)

Some patients experience intermittent, self-resolving episodes before a full attack:

• Transient blurred vision
• Intermittent haloes around lights (especially in evening/dim light)
• Mild brow ache or headache
• Resolution with sleep or bright light (pupil constriction opens angle)

Signs

Affected Eye Examination Findings

Fellow Eye Examination

• Shallow anterior chamber: Same anatomical predisposition
• Normal pupil reactions: Unless bilateral attack (rare)
• Normal IOP: Typically unaffected
• Narrow angle on gonioscopy: Confirms bilateral risk

The "Van Herick" Technique (Peripheral Anterior Chamber Depth Assessment)

A simple slit-lamp technique to assess anterior chamber depth:

Red Flags

[!DANGER] Red Flags — Immediate Ophthalmology Referral Required:

• Severe eye pain with fixed, mid-dilated pupil
• Sudden visual loss with red eye
• "Rock-hard" or "stony" eye on palpation
• Nausea/vomiting with headache and red eye
• Haloes around lights with acutely reduced vision
• IOP greater than 40 mmHg on measurement
• Hazy/cloudy cornea with unreactive pupil
• Headache with red eye in patient over 50 years

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5. Differential Diagnosis

Critical Differential Diagnoses

"Do Not Miss" Diagnoses

Systematic Approach to Acute Red Eye

Step 1: Assess Visual Acuity

• Significantly reduced → AACG, uveitis, keratitis, endophthalmitis

Step 2: Examine Pupil

• Fixed, mid-dilated → AACG (pathognomonic)
• Small (miotic) → Uveitis, cluster headache
• Normal, reactive → Conjunctivitis, episcleritis, scleritis

Step 3: Assess Cornea

• Hazy/cloudy → AACG, corneal infection
• Clear → Uveitis, scleritis, conjunctivitis

Step 4: Palpate Globe

• Rock-hard → AACG, neovascular glaucoma
• Normal tension → Other causes

Step 5: Measure IOP

• 40 mmHg → AACG (or other acute glaucoma)

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6. Clinical Examination

Structured Ophthalmic Examination

General Inspection

• Patient appears distressed, pale, diaphoretic
• May be actively vomiting
• May have hand over affected eye
• Appears systemically unwell (vs conjunctivitis patient appears comfortable)

Visual Acuity Assessment

• Test both eyes with patient's distance correction
• Often severely reduced: 6/60 or worse, counting fingers (CF), hand movements (HM)
• Record accurately; documents severity and provides baseline for recovery

External Eye Examination

Pupil Assessment

1. Size: Measure in mm; typically 4-6mm in AACG
2. Shape: Often oval or irregular (not round)
3. Direct response: Absent or minimal
4. Consensual response: Absent in affected eye
5. Compare with fellow eye: Fellow eye has normal reactions

Anterior Chamber Depth Assessment

Flashlight (Oblique Illumination) Test:

1. Shine penlight from temporal side, parallel to iris plane
2. Observe illumination of nasal iris

Van Herick Method (see Section 4)

Intraocular Pressure Measurement

Goldmann Applanation Tonometry (Gold Standard):

• Requires slit lamp, fluorescein, topical anaesthetic
• Normal: 10-21 mmHg
• AACG: Typically > 40 mmHg, often 50-80 mmHg

Portable/Handheld Tonometry:

• Tonopen, iCare: Useful in ED/primary care
• Acceptable accuracy for diagnosis

Digital Palpation (When Tonometry Unavailable):

• Compare tension of affected vs fellow eye
• "Rock-hard" vs normal = highly suggestive
• Sensitivity approximately 80% for IOP > 40 mmHg

Fundoscopy

• May be difficult due to corneal haze
• Look for optic disc cupping if view possible
• Assess for previous glaucomatous damage

Specialist Examination

Gonioscopy

Direct visualisation of the iridocorneal angle using a gonioscopy lens:

Shaffer Grading System:

In acute attack: Grade 0 angle (closed) due to iridotrabecular apposition

Anterior Segment OCT (AS-OCT)

• Non-contact imaging of angle anatomy
• Quantifies anterior chamber depth, angle opening distance
• Useful for screening and follow-up
• Can image through mild corneal oedema [23]

Ultrasound Biomicroscopy (UBM)

• High-frequency ultrasound (35-50 MHz)
• Visualises structures posterior to iris (ciliary body, lens zonules)
• Essential for diagnosing plateau iris syndrome
• Can be performed through severe corneal oedema [22]

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7. Investigations

First-Line Investigations (Emergency Department)

Laboratory Investigations

Specialist Imaging

Diagnostic Criteria for Acute Angle Closure

Clinical Diagnosis Requires:

1. Symptoms: At least 2 of:

   • Ocular pain
   • Headache
   • Nausea and/or vomiting
   • Blurred vision
   • Haloes

2. Signs: All of:

   • IOP > 21 mmHg (usually > 40 mmHg)
   • Corneal oedema
   • Fixed, mid-dilated pupil
   • Shallow anterior chamber

3. Confirmation (specialist): Gonioscopy showing closed angle

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8. Management

Emergency Management Algorithm

┌─────────────────────────────────────────────────────────┐
│           SUSPECTED ACUTE ANGLE CLOSURE                │
│  (Severe eye pain + red eye + mid-dilated pupil)       │
└────────────────────────┬────────────────────────────────┘
                         │
                         ▼
┌─────────────────────────────────────────────────────────┐
│  IMMEDIATE ACTIONS (First 15 minutes)                   │
│  1. Position patient SUPINE (lens falls back)           │
│  2. Confirm diagnosis: VA, pupil, cornea, IOP           │
│  3. URGENT OPHTHALMOLOGY REFERRAL                       │
└────────────────────────┬────────────────────────────────┘
                         │
                         ▼
┌─────────────────────────────────────────────────────────┐
│  MEDICAL TREATMENT (Start immediately)                  │
│                                                         │
│  SYSTEMIC:                                              │
│  • Acetazolamide 500mg IV stat (or 250mg IV + 250mg PO)│
│  • Antiemetic: Ondansetron 4mg IV or Cyclizine 50mg IM │
│  • Analgesia: Paracetamol 1g IV; opioids if severe     │
│                                                         │
│  TOPICAL (to affected eye):                             │
│  • Timolol 0.5% - 1 drop                               │
│  • Brimonidine 0.2% - 1 drop                           │
│  • Prednisolone 1% - 1 drop (reduces inflammation)     │
│                                                         │
│  HOLD PILOCARPINE until IOP falling                     │
└────────────────────────┬────────────────────────────────┘
                         │
                         ▼
┌─────────────────────────────────────────────────────────┐
│  RE-ASSESS IOP after 30-60 minutes                      │
└──────────────┬────────────────────────┬─────────────────┘
               │                        │
        IOP improving           IOP not responding
               │                        │
               ▼                        ▼
┌──────────────────────────┐   ┌──────────────────────────┐
│  ADD PILOCARPINE         │   │  ESCALATE TREATMENT      │
│  2% - 1 drop q15min × 4  │   │  • IV Mannitol 1-2 g/kg  │
│                          │   │    over 45-60 min        │
│  (Iris sphincter now     │   │  • Cardiac monitoring    │
│   responsive as IOP ↓)   │   │  • Avoid in HF/renal imp│
│                          │   │  • Consider anterior     │
│                          │   │    chamber paracentesis  │
└──────────────┬───────────┘   └──────────────────────────┘
               │
               ▼
┌─────────────────────────────────────────────────────────┐
│  DEFINITIVE TREATMENT (within 24-48 hours)              │
│                                                         │
│  LASER PERIPHERAL IRIDOTOMY (LPI)                       │
│  • Performed once IOP controlled & cornea clearing      │
│  • Creates bypass for aqueous (relieves pupillary block)│
│  • BOTH EYES must be treated                            │
│                                                         │
│  OR                                                     │
│  CLEAR LENS EXTRACTION (patients > 50 with cataract)     │
│  • Evidence from EAGLE trial supports this approach     │
└─────────────────────────────────────────────────────────┘

Pharmacological Treatment Details

Systemic Agents

Topical Agents

Symptom Control

Definitive Treatment

Laser Peripheral Iridotomy (LPI)

Mechanism: Creates a full-thickness hole in the peripheral iris, allowing aqueous to bypass the pupillary block and flow directly from posterior to anterior chamber.

Procedure:

1. Topical anaesthesia
2. Miotic (pilocarpine) to thin peripheral iris
3. Nd:YAG or argon laser application to peripheral iris (usually superior)
4. Multiple pulses to create patent opening
5. Post-procedure: Topical steroid, IOP check at 1 hour

Success Rate: > 95% for relieving pupillary block

Complications:

• IOP spike (10-15%)
• Bleeding from iris
• Dysphotopsia (glare, visual symptoms) — less common with superior placement
• Closure requiring retreatment (5-10%)

Critical Point: LPI must be performed on BOTH eyes. The fellow eye has 50-75% risk of acute attack within 5-10 years if untreated. [8,10]

Timing: Ideally within 24-48 hours of attack, once IOP controlled and cornea sufficiently clear.

Early Clear Lens Extraction (EAGLE Trial Evidence)

The EAGLE (Effectiveness of Early Lens Extraction) trial demonstrated that in patients aged > 50 with primary angle closure (PAC) or PACG and cataract, early clear lens extraction was more effective than LPI for long-term IOP control and had better quality of life outcomes at 36 months. [9]

Indications for Early Lens Extraction:

• Age > 50 years
• PAC or PACG (not just PACS)
• Coexisting cataract
• Failed LPI
• Plateau iris (LPI alone insufficient)
• Persistent elevated IOP after LPI

Advantages over LPI:

• Eliminates lens-related component of angle closure
• Deepens anterior chamber permanently
• Reduces long-term medication requirement
• Addresses visual impairment from cataract

Surgical Iridectomy

Reserved for cases where LPI not possible:

• Persistent corneal oedema preventing laser
• Inadequate pupil dilation
• Laser equipment unavailable

Post-Attack Management

Long-Term IOP-Lowering Requirements

30-50% of patients require ongoing topical IOP-lowering medication after acute attack due to:

• Trabecular meshwork damage
• Peripheral anterior synechiae
• Pre-existing glaucoma

First-line options: Prostaglandin analogues (latanoprost), beta-blockers (timolol)

Surgical Options for Refractory Cases

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9. Complications

Immediate Complications (Hours)

Early Complications (Days to Weeks)

Late Complications (Months to Years)

Corneal Endothelial Damage

AACG causes significant corneal endothelial cell loss, proportional to duration and severity of attack. [21] Endothelial cell density may be reduced by 10-30% compared to normal eyes. This may affect:

• Long-term corneal clarity
• Future cataract surgery outcomes
• Risk of corneal decompensation

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10. Prognosis & Outcomes

Natural History (Untreated)

• Sustained IOP > 50 mmHg causes optic nerve damage within 2-24 hours
• Complete, permanent visual loss possible within 24-72 hours
• Corneal decompensation may occur
• Spontaneous resolution is RARE (unlike intermittent subacute attacks)

Outcomes with Treatment

Prognostic Factors

Good Prognosis

• Rapid recognition and treatment (less than 6 hours)
• IOP reduced to less than 25 mmHg within 4 hours
• Successful LPI to both eyes
• No pre-existing optic nerve damage
• Good baseline visual acuity before attack
• Young age

Poor Prognosis

• Delayed presentation (> 24-48 hours)
• Very high IOP (> 60 mmHg)
• Pre-existing glaucomatous optic neuropathy
• Significant corneal damage at presentation
• Failed initial medical treatment
• Recurrent attacks
• Advanced age with comorbidities

Long-Term Follow-Up Requirements

All patients require lifelong ophthalmology follow-up:

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11. Prevention & Screening

Primary Prevention

Identifying At-Risk Individuals

Routine eye examinations should assess anterior chamber depth, particularly in:

• Patients over 40 years
• Hypermetropic patients
• Asian, Inuit, or Chinese ethnicity
• Family history of angle closure glaucoma
• Before administering mydriatic drops

Prophylactic Laser Peripheral Iridotomy

Indications:

• Primary angle closure suspect (PACS) with very narrow angles
• Fellow eye after unilateral AACG (mandatory)
• Primary angle closure (PAC) diagnosed on routine examination
• Before cataract surgery in narrow-angle eyes

Evidence for Prophylactic LPI:

The ZAP (Zhongshan Angle-Closure Prevention) Trial randomised Chinese subjects with bilateral PACS to LPI in one eye. At 6-year and 14-year follow-up: [8]

• AACG attack rate was very low in both groups (less than 1%)
• LPI did not significantly reduce progression to PAC
• Conclusion: Routine prophylactic LPI for PACS may not be necessary in all cases; close observation is an alternative

Current Recommendations:

• Prophylactic LPI is ALWAYS indicated for the fellow eye after AACG
• LPI for PACS remains controversial; individualise based on risk factors
• LPI recommended for PAC (elevated IOP or PAS even without acute attack) [22]

Secondary Prevention

Medication Counselling

Patients with narrow angles or prior AACG should:

• Carry a warning card about their condition
• Inform all healthcare providers before any medication
• Avoid over-the-counter anticholinergics and decongestants
• Seek urgent review if experiencing prodromal symptoms

Patient Education

Teach patients to recognise warning symptoms:

• Blurred vision in dim lighting
• Haloes around lights
• Brow ache or mild eye pain
• Seek immediate attention if symptoms worsen

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12. Evidence & Guidelines

Key Clinical Guidelines

Landmark Trials

EAGLE Trial (Azuara-Blanco et al., 2016) [9]

• Design: Multicentre RCT; 419 patients with PAC/PACG (age > 50)
• Comparison: Clear lens extraction vs LPI
• Primary Outcome: IOP and quality of life at 36 months
• Key Finding: Clear lens extraction was more effective than LPI for long-term IOP control; better health-related quality of life
• Impact: Supports early lens extraction in PAC/PACG patients > 50 with coexisting cataract

ZAP Trial (He et al., 2019) [8]

• Design: Single-centre RCT; 889 Chinese subjects with bilateral PACS
• Comparison: Prophylactic LPI to one eye vs observation
• Primary Outcome: Development of PAC or AACG at 6 years (extended to 14 years)
• Key Finding: Very low progression rate in both groups; LPI did not significantly reduce conversion to PAC
• Impact: Questions routine prophylactic LPI in all PACS; close observation may be reasonable

Fellow Eye Studies (Ang et al., 2000) [10]

• Design: Prospective cohort; 75 fellow eyes after unilateral AACG
• Intervention: Prophylactic LPI to fellow eye
• Follow-up: Mean 6.4 years
• Key Finding: No cases of AACG in prophylactically treated fellow eyes; untreated historical controls had 50-75% attack rate
• Impact: Established mandatory prophylactic LPI to fellow eye

Evidence Strength for Key Interventions

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13. Exam-Focused Section

Common Viva Questions

Opening Question

Q: "Tell me about acute angle closure glaucoma."

Model Answer: "Acute angle closure glaucoma is an ophthalmic emergency characterised by rapid obstruction of aqueous humour outflow due to apposition of the peripheral iris to the trabecular meshwork, causing acute elevation of intraocular pressure typically above 40 mmHg.

The condition predominantly affects females over 60 years old, those of Asian ethnicity, and hypermetropic individuals — all related to anatomical predisposition including shallow anterior chamber and narrow drainage angle.

The classic presentation is the triad of severe unilateral eye pain, reduced vision, and nausea with vomiting. Pathognomonic signs include a fixed mid-dilated pupil, hazy cornea due to oedema, ciliary flush, and a rock-hard eye on palpation.

Emergency treatment involves positioning supine, intravenous acetazolamide 500mg, topical timolol and brimonidine, with pilocarpine added once IOP begins to fall. Definitive treatment is laser peripheral iridotomy, which must be performed on both eyes given the high risk to the fellow eye."

Follow-Up Questions

Q: "Why is pilocarpine only effective after IOP starts to fall?"

A: "When IOP exceeds 50-60 mmHg, the iris sphincter muscle becomes ischaemic and paralysed. Pilocarpine acts by stimulating the sphincter to constrict the pupil and pull the peripheral iris away from the trabecular meshwork. An ischaemic sphincter cannot respond to cholinergic stimulation. Only when IOP falls with systemic acetazolamide does iris perfusion improve sufficiently for pilocarpine to work."

Q: "What is the mechanism of pupillary block?"

A: "Pupillary block is the most common mechanism of angle closure, accounting for over 90% of cases. The lens and iris are in contact at the pupillary margin. Aqueous, produced by the ciliary body in the posterior chamber, cannot easily flow through this contact zone. This creates a pressure gradient with higher pressure in the posterior chamber, causing the peripheral iris to bow forward (iris bombé). The forward-bowed iris then apposes the trabecular meshwork, blocking drainage completely. The block is maximum at mid-dilation (3-5mm pupil), explaining why dim lighting precipitates attacks."

Q: "What is plateau iris syndrome and how is it managed differently?"

A: "Plateau iris syndrome occurs when the iris root is abnormally anteriorly inserted at the ciliary body. The central anterior chamber may appear normal in depth, but the peripheral angle is narrow due to the anatomical position of the iris root. On pupil dilation, the peripheral iris bunches up and occludes the angle even though there is no pupillary block. LPI alone is insufficient because the mechanism is not pupillary block. Laser peripheral iridoplasty (applying laser burns to the peripheral iris to shrink and thin it) is often required, or lens extraction which deepens the entire anterior chamber."

Q: "Describe the EAGLE trial and its implications."

A: "The EAGLE trial was a multicentre randomised controlled trial comparing clear lens extraction with laser peripheral iridotomy in 419 patients over 50 years with primary angle closure or primary angle closure glaucoma. At 36-month follow-up, clear lens extraction demonstrated superior IOP control and better health-related quality of life compared to LPI alone. The clinical implication is that early lens extraction should be considered as primary treatment in PAC/PACG patients over 50, particularly those with coexisting cataract, rather than LPI with subsequent cataract surgery if needed."

Common Mistakes That Fail Candidates

High-Yield Exam Facts

1. Epidemiology: Global PACG prevalence 0.5%; 20 million affected; responsible for 50% of glaucoma blindness despite being 26% of cases [12]

2. Demographics: Female:Male 3-4:1; peak > 60 years; highest in Inuit/Asian populations [12,13]

3. IOP Values: Normal 10-21 mmHg; AACG typically > 40 mmHg (often 50-80 mmHg)

4. Pupil Size: Mid-dilated = 4-6mm (not small like uveitis, not large like pharmacological mydriasis)

5. Fellow Eye Risk: 50-75% attack rate over 5-10 years without prophylactic LPI [10]

6. ZAP Trial: Showed very low progression from PACS to PAC/AACG; prophylactic LPI for PACS is now questioned [8]

7. EAGLE Trial: Clear lens extraction superior to LPI for PAC/PACG in patients > 50 years [9]

8. Medication Triggers: Anticholinergics (antipsychotics, tricyclics, antihistamines), sympathomimetics (pseudoephedrine), topiramate [18,19]

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14. Special Populations

Elderly Patients

• Higher risk of AACG due to lens thickening with age
• More likely to have comorbidities affecting treatment choice
• Mannitol requires careful use (cardiac, renal function)
• May have difficulty with postoperative care
• Higher risk of falls due to impaired vision
• Early lens extraction often preferred (addresses cataract simultaneously)

Asian Populations

• Higher prevalence of AACG (1.0-1.4% vs 0.1-0.4% in Caucasians) [12,14]
• Plateau iris more common
• May require more aggressive screening
• Lower threshold for prophylactic LPI in high-risk individuals

Patients with Cognitive Impairment

• May not report symptoms accurately
• Carers must be educated about warning signs
• Consider prophylactic LPI if narrow angles identified
• May need modified postoperative management

Medication-Related AACG

• Review all medications in patients with narrow angles
• Particular caution with:
  • Anticholinergics (oxybutynin, antihistamines)
  • Tricyclic antidepressants
  • "Topiramate (unique mechanism: ciliary body oedema)"
  • Perioperative anticholinergics
• Consider alternative medications where possible

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15. Patient/Layperson Explanation

What is Acute Angle Closure Glaucoma?

Acute angle closure glaucoma is a serious eye emergency that happens when the pressure inside your eye rises very suddenly. This can damage the nerve at the back of your eye (optic nerve) and cause permanent loss of vision if not treated quickly.

What Causes It?

Inside your eye, a clear fluid called aqueous humour is constantly being made and drained away. The drain is located at the "angle" where the coloured part of your eye (iris) meets the clear front part (cornea). In some people, this angle is very narrow. When the angle closes completely, the fluid cannot drain, pressure builds up rapidly, and this causes the symptoms.

Am I at Risk?

You are more likely to have this condition if you:

• Are over 60 years old
• Are female
• Are of Asian, Chinese, or Inuit descent
• Are long-sighted (wear "plus" glasses for distance)
• Have a family member who has had this condition
• Have been told you have "narrow angles"

Certain medications can trigger an attack in people at risk, including some cold and allergy medicines, some bladder medications, and some antidepressants. Always tell your doctor or pharmacist if you have been told you have narrow angles.

What are the Warning Signs?

Seek emergency help immediately if you experience:

• Sudden, severe pain in one eye
• Blurred vision that comes on quickly
• Seeing rainbow-coloured haloes around lights
• Red eye with severe pain
• Headache with nausea and vomiting (especially with a red eye)
• The eye feeling very hard when you press on it gently

These symptoms are an emergency. Do not wait — go to your nearest Emergency Department or call for an ambulance.

How is it Treated?

Emergency Treatment:

• Medicines are given immediately to lower the pressure (eye drops and an injection)
• You may be asked to lie flat
• Medicine to stop sickness and pain will also be given

Laser Treatment (Iridotomy):

• Once the pressure is controlled, a laser is used to make a tiny hole in the coloured part of your eye
• This creates a new pathway for the fluid to drain
• It is done on BOTH eyes because the other eye is also at risk

Sometimes Surgery:

• In some cases, removing the lens of the eye (like a cataract operation) is the best treatment

What to Expect After Treatment

• Most people recover good vision if treated within a few hours
• You will need regular check-ups with an eye doctor for the rest of your life
• You may need to use eye drops long-term
• You should carry a card or wear a bracelet alerting medical staff to your condition

How Can I Prevent Future Attacks?

• Attend all your eye appointments
• Use your medications as prescribed
• Avoid medications that can trigger attacks (ask your doctor or pharmacist)
• Tell all your doctors about your eye condition
• Seek urgent help if you experience any warning symptoms

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17. References

1. Weinreb RN, Aung T, Medeiros FA. The pathophysiology and treatment of glaucoma: a review. JAMA. 2014;311(18):1901-1911. doi:10.1001/jama.2014.3192

2. European Glaucoma Society. Terminology and Guidelines for Glaucoma. 5th ed. Savona, Italy: PubliComm; 2020.

3. Wright C, Tawfik MA, Waisbourd M, Katz LJ. Primary angle-closure glaucoma: an update. Acta Ophthalmol. 2016;94(3):217-225. doi:10.1111/aos.12784

4. Chan PP, Pang JC, Tham CC. Acute primary angle closure-treatment strategies, evidences and economical considerations. Eye (Lond). 2019;33(1):110-119. doi:10.1038/s41433-018-0271-0 [PMID: 30467424]

5. Lowe RF. Aetiology of the anatomical basis for primary angle-closure glaucoma. Biometrical comparisons between normal eyes and eyes with primary angle-closure glaucoma. Br J Ophthalmol. 1970;54(3):161-169. doi:10.1136/bjo.54.3.161

6. Saw SM, Gazzard G, Friedman DS. Interventions for angle-closure glaucoma: an evidence-based update. Ophthalmology. 2003;110(10):1869-1878. doi:10.1016/S0161-6420(03)00540-9

7. Chen PP. Blindness in patients with treated open-angle glaucoma. Ophthalmology. 2003;110(4):726-733. doi:10.1016/S0161-6420(02)01974-7

8. He M, Jiang Y, Huang S, et al. Laser peripheral iridotomy for the prevention of angle closure: a single-centre, randomised controlled trial. Lancet. 2019;393(10181):1609-1618. doi:10.1016/S0140-6736(18)32607-2 [PMID: 30878226]

9. Azuara-Blanco A, Burr J, Ramsay C, 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. doi:10.1016/S0140-6736(16)30956-4 [PMID: 27707498]

10. Ang LP, Aung T, Chew PT. Acute primary angle closure in an Asian population: long-term outcome of the fellow eye after prophylactic laser peripheral iridotomy. Ophthalmology. 2000;107(11):2092-2096. doi:10.1016/s0161-6420(00)00449-1 [PMID: 11054339]

11. Gupta D, Chen PP. Glaucoma. Am Fam Physician. 2016;93(8):668-674. [PMID: 27175839]

12. Tham YC, Li X, Wong TY, Quigley HA, Aung T, Cheng CY. Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis. Ophthalmology. 2014;121(11):2081-2090. doi:10.1016/j.ophtha.2014.05.013 [PMID: 24974815]

13. Quigley HA, Broman AT. The number of people with glaucoma worldwide in 2010 and 2020. Br J Ophthalmol. 2006;90(3):262-267. doi:10.1136/bjo.2005.081224 [PMID: 16488940]

14. Foster PJ, Oen FT, Machin D, et al. The prevalence of glaucoma in Chinese residents of Singapore: a cross-sectional population survey of the Tanjong Pagar district. Arch Ophthalmol. 2000;118(8):1105-1111. doi:10.1001/archopht.118.8.1105

15. He M, Foster PJ, Ge J, et al. Prevalence and clinical characteristics of glaucoma in adult Chinese: a population-based study in Liwan District, Guangzhou. Invest Ophthalmol Vis Sci. 2006;47(7):2782-2788. doi:10.1167/iovs.06-0051

16. Bourne RR, Sukudom P, Foster PJ, et al. Prevalence of glaucoma in Thailand: a population based survey in Rom Klao District, Bangkok. Br J Ophthalmol. 2003;87(9):1069-1074. doi:10.1136/bjo.87.9.1069

17. Lowe RF. Primary angle-closure glaucoma: family histories and anterior chamber depths. Br J Ophthalmol. 1964;48(4):191-195. doi:10.1136/bjo.48.4.191

18. Lachkar Y, Bouassida W. Drug-induced acute angle closure glaucoma. Curr Opin Ophthalmol. 2007;18(2):129-133. doi:10.1097/ICU.0b013e32808738d5

19. Huff ML, Liu CA, Dhillon N, et al. Acute angle closure glaucoma precipitated by homeopathic eyedrops containing Atropa belladonna. Am J Emerg Med. 2022;54:288.e5-288.e7. doi:10.1016/j.ajem.2021.10.006 [PMID: 34776281]

20. Weinreb RN, Khaw PT. Primary open-angle glaucoma. Lancet. 2004;363(9422):1711-1720. doi:10.1016/S0140-6736(04)16257-0

21. Yeom H, Lee SU, Lee SB. Corneal endothelial cell loss after phacoemulsification in eyes with a prior acute angle-closure attack. Korean J Ophthalmol. 2020;34(6):470-476. doi:10.3341/kjo.2020.0078 [PMID: 33307602]

22. Filippopoulos T, Thau A, Bhai H. Rethinking Prophylactic Laser Peripheral Iridotomy in Primary Angle-Closure Suspects: A Review. Ophthalmol Glaucoma. 2023;6(6):542-554. doi:10.1016/j.ogla.2023.05.002 [PMID: 37321374]

23. Nongpiur ME, Gong T, Lee HK, et al. Subgrouping of primary angle-closure suspects based on anterior segment optical coherence tomography parameters. Ophthalmology. 2013;120(12):2525-2531. doi:10.1016/j.ophtha.2013.05.028

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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. Do not delay treatment. Call emergency services or attend your nearest Emergency Department immediately.