PanOph

Primary angle-closure glaucoma

Glaucoma

Key Points

  • •PACG accounts for 50% of global bilateral glaucoma blindness despite being less common than POAG — early detection is critical
  • •Pupillary block is the mechanism in ~75% of cases; LPI is the definitive treatment for acute angle closure
  • •In acute angle closure with IOP >50 mmHg, pilocarpine is ineffective (ischemic sphincter) — lower IOP first with timolol, apraclonidine, and systemic acetazolamide/mannitol
  • •Always treat the fellow eye with prophylactic LPI — untreated risk of acute attack is 40–80% over 5–10 years
  • •EAGLE trial (Lancet 2016): Early clear lens extraction is superior to LPI for PAC/PACG with IOP >30 mmHg (21% vs 61% needing further treatment)
1. Definition

Primary angle-closure glaucoma (PACG) is a form of glaucoma characterized by appositional or synechial closure of the anterior chamber angle by the peripheral iris, resulting in obstruction of aqueous outflow, elevated intraocular pressure, and glaucomatous optic neuropathy with visual field loss. It encompasses a spectrum from primary angle-closure suspect (PACS) to acute angle-closure crisis (AAO PPP Primary Angle Closure Disease 2020).

2. Epidemiology

PACG affects approximately 23 million people worldwide and is responsible for nearly 50% of global glaucoma-related bilateral blindness despite being less prevalent than POAG. Highest prevalence in East Asian and Southeast Asian populations: 1.0–1.5% in Chinese, 2.3% in Mongolians, 2.5% in Inuit populations. Lower prevalence in European (~0.4%) and African (~0.6%) populations. Female-to-male ratio is 2–4:1. Peak incidence is in the 6th–7th decades. Hypermetropes are disproportionately affected. PACS (narrow angles without glaucomatous damage) affects 3–5% of Asian populations over age 40. The Liwan Eye Study, Handan Eye Study, and Singapore Epidemiology of Eye Diseases Study provided key Asian data.

3. Aetiology and causes

PACG results from anatomical predisposition and dynamic factors:

Anatomical risk factors:

  • Short axial length (=<22 mm==) — shallow anterior chamber
  • Thick, anteriorly positioned crystalline lens — increases lens vault
  • Shallow anterior chamber depth (=<2.5 mm== centrally)
  • Short anterior chamber width
  • Small corneal diameter
  • Plateau iris configuration — anteriorly positioned ciliary processes push peripheral iris forward

Mechanisms of angle closure (multiple may coexist):

  1. Pupillary block (most common, ~75%): Resistance to aqueous flow at the iris-lens interface causes pressure gradient, bowing iris forward (iris bombé)
  2. Plateau iris: Large or anteriorly rotated ciliary processes push peripheral iris into the angle despite patent iridotomy
  3. Lens-induced: Intumescent or subluxated lens
  4. Malignant glaucoma (aqueous misdirection): Posterior diversion of aqueous into vitreous

Precipitating factors for acute attack: Dim illumination (mid-dilation), emotional stress, prone position, sympathomimetics, anticholinergics, topiramate (bilateral angle closure via ciliary body edema).

4. Pathogenesis

The pathogenesis involves progressive narrowing and eventual closure of the drainage angle:

  1. Pupillary block mechanism: Aqueous humor produced by the ciliary body must pass through the pupil. In susceptible eyes, the lens-iris contact area is increased, creating resistance to forward flow. A posterior-to-anterior pressure gradient develops across the iris, causing the peripheral iris to bow forward (iris bombé) and appose the trabecular meshwork.
  2. Appositional closure: Initially, the iris merely touches the TM (appositional closure), and angle opening can be achieved by indentation gonioscopy, pilocarpine, or laser iridotomy.
  3. Synechial closure: With prolonged or repeated appositional contact, the iris adheres to the TM forming peripheral anterior synechiae (PAS). PAS cause permanent angle closure that is not reversible with iridotomy.
  4. Trabecular damage: Even after angle re-opening, previously synechially closed TM may be dysfunctional due to inflammatory damage, leading to persistently elevated IOP.
  5. Acute angle-closure crisis: Sudden, complete pupillary block causes rapid IOP elevation (often 50–80 mmHg), ischemic damage to the iris (sphincter paralysis, iris atrophy), TM inflammation and edema, and acute optic nerve damage. Corneal endothelial damage may occur. Glaukomflecken (anterior subcapsular lens opacities) visible after the attack resolves are pathognomonic of a prior acute attack.
  6. Chronic angle closure: Gradual, asymptomatic synechial closure of the angle ('creeping angle closure'), mimicking POAG in presentation.
5. Classification

ISGEO classification (International Society of Geographical and Epidemiological Ophthalmology):

  1. Primary angle-closure suspect (PACS): Appositional contact between peripheral iris and posterior TM in ≥2 quadrants on gonioscopy. No PAS, normal IOP, no glaucomatous damage. Previously called 'narrow angles' or 'occludable angles.'
  2. Primary angle closure (PAC): Appositional or synechial angle closure with elevated IOP and/or PAS, BUT no glaucomatous optic neuropathy. May present as acute, intermittent, or chronic.
  3. Primary angle-closure glaucoma (PACG): Angle closure with glaucomatous optic neuropathy (disc and/or field changes). May be acute, subacute/intermittent, or chronic.

Clinical presentations:

  • Acute angle-closure crisis: Sudden onset, symptomatic, IOP usually >40 mmHg
  • Subacute/Intermittent: Repeated episodes of angle closure that resolve spontaneously; may cause subtle PAS
  • Chronic angle closure: Gradual, asymptomatic synechial closure; may present like POAG
  • Plateau iris syndrome: Recurrent angle closure despite patent laser peripheral iridotomy (LPI); confirmed by UBM showing anteriorly rotated ciliary processes

Spaeth gonioscopy classification: Iris insertion, angular approach, iris configuration (steep/regular/queer), degree of pigmentation.

6. Risk factors and associations

Ocular risk factors:

  • Hypermetropia (>+2.00 D): Shorter axial length, shallower AC
  • Shallow anterior chamber depth: =<2.5 mm== centrally (van Herick grade ≤2 on slit lamp)
  • Short axial length: =<21.5 mm==
  • Increased lens thickness and anterior lens vault: Lens vault is the strongest predictor on AS-OCT
  • Small corneal diameter: =<11 mm==
  • Plateau iris configuration
  • Nanophthalmos: Very small eyes with thick sclera

Demographic risk factors:

  • East Asian / Southeast Asian ethnicity: 2–3x higher risk than European descent
  • Female sex: 2–4x higher risk (shorter axial length, shallower AC)
  • Age >50 years: Progressive lens thickening with age
  • Family history: 3.5x increased risk with affected first-degree relative
  • Inuit / Eskimo populations: Highest reported prevalence worldwide

Pharmacological precipitants:

  • Topical mydriatics (tropicamide, phenylephrine) — mid-dilated pupil is highest risk
  • Systemic anticholinergics (atropine, hyoscine, ipratropium)
  • Sympathomimetics (ephedrine, pseudoephedrine)
  • Topiramate, sulfonamides (uveal effusion mechanism — not pupillary block)
  • Selective serotonin reuptake inhibitors (SSRIs) — rare
7. Clinical features

Acute angle-closure crisis:

Symptoms: Sudden onset severe unilateral eye pain, headache (often frontal/temporal), nausea and vomiting (vagal response to acute IOP rise), blurred vision, halos around lights (corneal edema), red eye.

Signs:

  • IOP markedly elevated (often 50–80 mmHg; eye feels rock-hard on palpation)
  • Corneal edema (epithelial and stromal) — hazy cornea
  • Mid-dilated, vertically oval, fixed pupil (iris sphincter ischemia)
  • Shallow anterior chamber with flare and cells
  • Conjunctival and ciliary injection
  • Closed angle on gonioscopy (if cornea clear enough)
  • Glaukomflecken: Small grey-white anterior subcapsular lens opacities (pathognomonic of prior acute attack — iris pigment on lens from sphincter necrosis)
  • Iris atrophy (sectoral, due to ischemia) — visible after attack resolves
  • Fellow eye: Shallow AC, narrow angle (examine to confirm predisposition)

Chronic angle closure:

  • Often asymptomatic, similar to POAG
  • Elevated IOP, PAS on gonioscopy, optic disc cupping, visual field defects
  • No corneal edema or acute symptoms

Subacute/Intermittent:

  • Recurrent episodes of blurred vision, halos, mild eye ache — especially in evening/dim light
  • Self-resolving as pupil constricts (sleep, bright light)
8. Investigations

Gonioscopy (essential for diagnosis):

  • Direct gonioscopy (Koeppe lens): Wider field of view, performed supine
  • Indirect gonioscopy (Goldmann, Zeiss/Posner 4-mirror): Performed at slit lamp; indentation gonioscopy distinguishes appositional (opens with indentation) from synechial (does not open) closure
  • Grade using Shaffer, Spaeth, or Scheie systems
  • Document: iris insertion, degree of angle opening, PAS extent, pigmentation, neovascularization

Anterior segment imaging:

  • AS-OCT (Visante, CASIA): Quantitative assessment of ACA, AOD (angle opening distance), TISA (trabecular-iris space area), lens vault, ACD
  • UBM (ultrasound biomicroscopy, 50 MHz): Gold standard for plateau iris diagnosis; visualizes ciliary body position, iris-lens relationship, and structures behind the iris that OCT cannot image

IOP measurement:

  • Goldmann applanation tonometry: IOP typically >40 mmHg in acute attack
  • Tonopen or iCare if corneal edema prevents GAT

Optic disc and RNFL:

  • Dilated fundus exam (after iridotomy is performed — never dilate a closed angle before iridotomy)
  • OCT RNFL and ONH analysis
  • Disc photography

Visual field testing:

  • Humphrey 24-2 or 30-2; may show diffuse or localized defects
  • Field loss may be more diffuse in PACG compared to POAG

Biometry:

  • A-scan ultrasonography: Axial length, ACD, lens thickness
  • IOLMaster/Lenstar: Non-contact biometry

Provacative tests (largely historical):

  • Dark room prone provocative test: IOP rise >8 mmHg considered positive
  • Pharmacological mydriasis test: No longer routinely performed due to risk
9. Differential diagnosis
  1. Secondary angle-closure glaucomas:
  • Neovascular glaucoma: New vessels on iris (rubeosis) and angle; history of retinal ischemia (diabetic retinopathy, CRVO)
  • Phacomorphic glaucoma: Intumescent cataract pushing iris forward; unilateral; lens obviously swollen
  • Inflammatory: Posterior synechiae causing iris bombé; cells and flare prominent; look for keratic precipitates
  • ICE syndrome: Iris abnormalities, corneal endothelial changes, PAS extending anterior to Schwalbe's line; young females
  • Aqueous misdirection (malignant glaucoma): Uniformly shallow AC (axial and peripheral); occurs post-surgery
  1. Acute conditions mimicking acute angle closure:
  • Acute anterior uveitis: Pain and redness but IOP usually normal or low; deep AC; miotic pupil; keratic precipitates
  • Acute conjunctivitis: Red eye with discharge; no IOP elevation; clear cornea; deep AC
  • Corneal hydrops (keratoconus): Acute corneal edema but no IOP elevation; history of KC
  1. POAG: Open angles on gonioscopy; gonioscopy is mandatory to differentiate
  2. Phacolytic glaucoma: Open angle; hypermature cataract; large keratic precipitates from lens protein leakage
  3. Topiramate-induced bilateral angle closure: Bilateral simultaneous onset; ciliary body edema on UBM; not responsive to LPI; resolves with drug cessation
10. Complications

Complications of acute angle-closure crisis:

  • Permanent synechial angle closure and chronic IOP elevation
  • Iris sphincter damage: Fixed, dilated or irregular pupil; iris atrophy
  • Glaukomflecken: Anterior subcapsular lens opacities (do not affect vision but indicate prior attack)
  • Cataract acceleration: Lens damage from ischemia during acute attack
  • Optic nerve damage: Acute ischemia can cause severe, irreversible optic neuropathy; risk of 'wipeout' (sudden complete visual loss)
  • Corneal decompensation: Endothelial cell loss from pressure-induced damage
  • Central retinal vein occlusion (rare, from markedly elevated IOP)
  • Fellow eye attack: 40–80% risk over 5–10 years if prophylactic LPI not performed

Complications of chronic PACG:

  • Progressive visual field loss similar to POAG
  • Advanced optic disc cupping
  • Bilateral blindness (higher rate than POAG globally due to late presentation)

Complications of treatment:

  • LPI: Transient IOP spike, hyphema, posterior synechiae at iridotomy site, dysphotopsia (glare/ghost images in ~3%), closure of iridotomy requiring retreatment
  • Surgical iridectomy: Cataract progression, hyphema
  • Lens extraction complications: Standard cataract surgery risks but higher risk of zonular weakness, shallow AC intraoperatively
11. Management

ACUTE ANGLE-CLOSURE CRISIS — Medical emergency:

Immediate medical management (aim to lower IOP and break pupillary block):

  1. Supine position (allows lens to fall back)
  2. Topical medications:
  • Timolol 0.5% ×1 dose (reduce aqueous production)
  • Pilocarpine 2% every 15 min ×2 doses ONLY AFTER IOP starts to fall (ineffective on ischemic sphincter at IOP >50 mmHg — wait until IOP <50)
  • Apraclonidine 1% ×1 dose or brimonidine 0.2%
  • Prednisolone acetate 1% every 15 min ×4 doses then hourly (reduce inflammation)
  1. Systemic medications:
  • Acetazolamide 500 mg IV stat or 500 mg PO stat (if no sulfa allergy, renal impairment)
  • Oral glycerol 50% (1–1.5 g/kg) or IV mannitol 20% (1–2 g/kg over 45 min) — for refractory IOP elevation; avoid glycerol in diabetics
  1. Analgesics and antiemetics as needed

Definitive treatment:

  • Laser peripheral iridotomy (LPI): Nd:YAG laser (preferred) or argon laser. Performed once cornea clears and IOP controlled. Place at 11 or 1 o'clock (covered by upper lid to minimize dysphotopsia). Full-thickness iridotomy confirmed by transillumination and visible lens capsule.
  • Fellow eye prophylactic LPI: Should be performed at earliest opportunity (40–80% risk of attack in untreated fellow eye)

CHRONIC PACG management:

  • LPI if not already performed
  • If IOP remains elevated after LPI: Topical medications (PGAs, beta-blockers, CAIs — same as POAG)
  • Lens extraction: EAGLE study (Lancet 2016) showed clear lens extraction superior to LPI for PACG and PAC with IOP >30 mmHg; lowers IOP by deepening AC; consider early in patients with visually significant cataract or refractory IOP
  • Laser iridoplasty (argon/diode): For plateau iris syndrome; long burns to peripheral iris to contract and pull it away from angle
  • Trabeculectomy with MMC or tube shunt surgery: When medical therapy and lens extraction fail; higher complication rate in PACG than POAG (shallow AC, malignant glaucoma risk)
  • Goniosynechialysis: Stripping of PAS; most effective when PAS are recent (=<6–12 months==); often combined with cataract surgery
12. Prognosis

PACG carries a worse visual prognosis than POAG globally, largely due to acute presentations and late diagnosis in endemic regions.

Acute angle-closure crisis:

  • If treated within 24–48 hours: Good prognosis for IOP control after LPI; residual optic nerve damage depends on severity and duration of attack
  • Delayed treatment (>72 hours): Significant risk of permanent vision loss, chronic IOP elevation requiring surgery
  • Up to 50% of eyes may require additional IOP-lowering treatment after successful LPI due to synechial damage to the TM

Chronic PACG:

  • More likely to present with advanced disease than POAG
  • Responds well to lens extraction (EAGLE study: mean IOP reduction of ~6 mmHg with clear lens extraction vs ~2 mmHg with LPI at 3 years)
  • Higher rate of surgical complications compared to POAG

Fellow eye:

  • 40–80% risk of acute attack in 5–10 years without prophylactic LPI
  • Prophylactic LPI reduces risk to =<1%==

PACS (narrow angles without damage):

  • ZAP trial (2022): Prophylactic LPI in PACS did not significantly reduce progression to PAC over 6 years (~7% in both groups); routine LPI for all PACS is no longer recommended — monitoring is reasonable

Global burden: PACG accounts for ~50% of bilateral glaucoma blindness worldwide despite representing only ~25% of glaucoma cases, underscoring the importance of early detection and treatment.

Clinical Pearls

1
Never dilate a patient with a shallow anterior chamber (van Herick grade ≤2) before performing gonioscopy — if angles are narrow and iridotomy has not been done, dilation can precipitate an acute angle-closure crisis.
2
In an acute attack with IOP >50 mmHg, pilocarpine will NOT work because the iris sphincter is ischemic and paralyzed — lower IOP first with timolol, apraclonidine, and systemic acetazolamide/mannitol, then instill pilocarpine once IOP drops below ~50 mmHg.
3
Always examine and treat the fellow eye — prophylactic LPI reduces the risk of acute attack from 40–80% to <1% and should be performed at the earliest opportunity.
4
The EAGLE study (Lancet 2016) is a landmark trial: early clear lens extraction was more effective and cost-effective than LPI for managing PAC/PACG with IOP >30 mmHg — lens extraction should be considered early, especially in older patients.
5
Glaukomflecken (grey-white anterior subcapsular lens opacities) are pathognomonic of a prior acute angle-closure attack and can be the only clinical evidence of a previous episode — always look for them.
6
Topiramate can cause bilateral angle closure via ciliary body edema (not pupillary block) — it does NOT respond to LPI; management is drug cessation + cycloplegia + topical steroids.
7
The ZAP trial (2022) showed that prophylactic LPI in PACS did not reduce progression to PAC — routine LPI for all narrow angles is no longer recommended; monitoring is acceptable.

Oral-exam questions

  • Why is pilocarpine ineffective in acute angle closure with IOP >50 mmHg? — The iris sphincter muscle is ischemic and paralyzed at very high IOPs. Pilocarpine cannot constrict a non-functioning sphincter. Lower IOP first with timolol, apraclonidine, and systemic acetazolamide/mannitol, then use pilocarpine once IOP drops below ~50 mmHg.
  • What is the risk to the fellow eye in acute angle closure? — 40–80% risk of acute attack in 5–10 years without prophylactic LPI. Prophylactic LPI reduces this risk to =<1%==. Always treat the fellow eye at the earliest opportunity.
  • What are glaukomflecken and what do they indicate? — Small grey-white anterior subcapsular lens opacities from focal lens epithelial necrosis during the acute attack. They are pathognomonic of a prior acute angle-closure episode and persist permanently.
  • What did the EAGLE study show? — Early clear lens extraction was superior to LPI for PAC/PACG with IOP ≥30 mmHg: only 21% needed further treatment vs 61% with LPI at 3 years. Mean IOP was 1.18 mmHg lower. CLE was also more cost-effective (EAGLE, Lancet 2016).
  • What is plateau iris and how is it diagnosed? — Recurrent angle closure despite patent LPI. Diagnosed by UBM showing anteriorly rotated ciliary processes pushing peripheral iris forward. Treated with argon laser iridoplasty.
  • How does topiramate cause angle closure? — Via ciliary body edema and anterior rotation (uveal effusion mechanism), causing bilateral simultaneous angle closure. It is NOT pupillary block and does NOT respond to LPI. Management: stop topiramate + cycloplegics + topical steroids.
  • What did the ZAP trial (2022) show about prophylactic LPI for narrow angles (PACS)? — Prophylactic LPI did not significantly reduce progression to PAC over 6 years (~7% in both groups). Routine LPI for all PACS is no longer recommended; monitoring is a reasonable strategy.

Mnemonics

ACGT (Acute Closure — Get Treatment)

A — Acetazolamide IV 500 mg (first systemic) C — Corneal edema = don't use pilocarpine yet (IOP >50) G — Get LPI once IOP controlled + cornea clears T — Treat the FELLOW EYE with prophylactic LPI

EAGLE Numbers

E — Early lens extraction A — Age ≥50 years, IOP ≥30 mmHg (inclusion) G — Got 21% needing further Rx (vs 61% with LPI) L — Lancet 2016 E — Evidence for CLE over LPI in PAC/PACG

Comparison Tables

ISGEO Classification of Primary Angle Closure Disease
Angle closure
PACS
Appositional contact ≥2 quadrants
PAC
Appositional or synechial
PACG
Appositional or synechial
PAS
PACS
Absent
PAC
May be present
PACG
Present
IOP
PACS
Normal
PAC
Elevated and/or PAS
PACG
Elevated
Optic disc
PACS
Normal
PAC
Normal
PACG
Glaucomatous cupping
Visual field
PACS
Normal
PAC
Normal
PACG
Glaucomatous defects
Management
PACS
Monitor (ZAP trial: LPI not needed routinely)
PAC
LPI ± medications
PACG
LPI + medications ± lens extraction ± surgery
Prognosis
PACS
Most do not progress
PAC
Risk of acute attack if untreated
PACG
Worse than POAG globally
Acute Angle Closure: Emergency Drug Protocol
Timolol 0.5%
Mechanism
Reduces aqueous production
Dose
1 drop × 1
Key Note
First topical agent; acts immediately
Apraclonidine 1%
Mechanism
Reduces aqueous production
Dose
1 drop × 1
Key Note
Alpha-2 agonist; alternative to brimonidine
Pilocarpine 2%
Mechanism
Constricts pupil, breaks pupillary block
Dose
1 drop q15min × 2
Key Note
ONLY after IOP <50 mmHg (ischemic sphincter)
Prednisolone 1%
Mechanism
Reduces inflammation
Dose
q15min × 4, then hourly
Key Note
Essential to control inflammation before LPI
Acetazolamide
Mechanism
Systemic CAI
Dose
500 mg IV/PO stat
Key Note
Rapid IOP reduction; avoid in sulfa allergy
Mannitol 20%
Mechanism
Osmotic agent
Dose
1–2 g/kg IV over 45 min
Key Note
Refractory cases; contraindicated in CHF/renal failure
LPI vs Clear Lens Extraction for Angle Closure (EAGLE Trial)
Mechanism
Laser Peripheral Iridotomy (LPI)
Bypasses pupillary block
Clear Lens Extraction (CLE)
Deepens AC by removing thick lens
IOP reduction at 3 yrs
Laser Peripheral Iridotomy (LPI)
~2 mmHg
Clear Lens Extraction (CLE)
~6 mmHg
Need for further Rx at 3 yrs
Laser Peripheral Iridotomy (LPI)
61%
Clear Lens Extraction (CLE)
21%
Cost-effectiveness
Laser Peripheral Iridotomy (LPI)
Less cost-effective
Clear Lens Extraction (CLE)
More cost-effective
Invasiveness
Laser Peripheral Iridotomy (LPI)
Outpatient laser
Clear Lens Extraction (CLE)
Intraocular surgery
Best indication
Laser Peripheral Iridotomy (LPI)
PACS, mild PAC, young patients
Clear Lens Extraction (CLE)
PACG/PAC with IOP >30, age ≥50, cataract
Evidence
Laser Peripheral Iridotomy (LPI)
Traditional first-line
Clear Lens Extraction (CLE)
EAGLE trial (Lancet 2016) supports superiority

Self-Assessment (5)

MCQ

A 60-year-old woman presents with sudden onset severe right eye pain, nausea, vomiting, and halos around lights. IOP is 62 mmHg with a hazy cornea and mid-dilated fixed pupil. Which drug should NOT be instilled first?

MCQ

According to the EAGLE trial, early clear lens extraction was superior to LPI for PACG. What was the key inclusion criterion?

MCQ

What is the risk of an acute angle-closure attack in the untreated fellow eye of a patient who has had an acute attack?

MCQ

A patient with narrow angles has recurrent angle closure episodes despite a patent laser iridotomy. UBM shows anteriorly rotated ciliary processes. What is the diagnosis and treatment?

MCQ

A patient taking topiramate for migraines presents with bilateral simultaneous angle closure. What is the correct management?

References

  1. AAO Preferred Practice Pattern: Primary Angle Closure Disease (2020)
  2. 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.
  3. He M, Jiang Y, Huang S, et al. Laser peripheral iridotomy for the prevention of angle closure: a single-centre, randomised controlled trial (ZAP). Lancet. 2019;393(10181):1609-1618.
  4. Shields MB. Textbook of Glaucoma, 6th Edition. Lippincott Williams & Wilkins.
  5. Stamper RL, Lieberman MF, Drake MV. Becker-Shaffer's Diagnosis and Therapy of the Glaucomas, 11th Edition.
  6. Ehlers JP, Shah CP. The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease, 8th Edition.

Related Content

EAGLE — Effectiveness of Early Lens Extraction for PACGAGIS — Advanced Glaucoma Intervention StudyPrimary Open-Angle GlaucomaNeovascular GlaucomaCongenital GlaucomaPseudoexfoliation GlaucomaAcute Angle Closure
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