Primary Angle Closure Glaucomas Flashcards

What is primary angle closure glaucoma (PACG)?

Glaucoma caused by closure of the anterior chamber angle due to an anatomical predisposition, resulting in impaired aqueous outflow and optic nerve damage (GON).

What is the difference between primary and secondary angle closure glaucoma?

Primary: Due to anatomical predisposition with no other ocular pathology causing closure. Secondary: Due to another pathological process such as neovascularization, uveitis, lens-induced glaucoma, or tumors.

What is Primary Angle Closure Suspect (PACS)?

Patients with anatomically narrow angles but no glaucoma, no optic nerve damage, and no visual field loss. They require close monitoring and may receive prophylactic treatment.

Approximately how many people worldwide have PACG?

Approximately 16 million people.

How common is PACG compared with POAG?

Approximately one-third as common as primary open-angle glaucoma.

Where is PACG most prevalent?

Asia, accounting for 86% of worldwide PACG cases; 48% in China, 23.9% in India, and 14.1% in Southeast Asia.

Which ethnic groups have the highest risk of PACG?

Asian and Inuit.

Which ethnic group has the lowest risk?

People of European and African descent.

How much more common is PACG in Inuit populations compared with Caucasians?

Approximately 20–40 times more common.

What are the major risk factors for primary angle closure glaucoma?

Family history, older age, female sex (4:1 female:male), hyperopia, Asian ethnicity, Inuit ethnicity, short axial length, thick anterior lens, shallow anterior chamber, and narrow angle.

Does myopia eliminate the risk of angle closure?

No, although uncommon, myopic patients can still develop PACG.

What is the most common mechanism of PACG?

Relative pupillary block, accounting for 90% of cases.

What is relative pupillary block?

The iris contacts the anterior lens surface, creating resistance to aqueous movement from the posterior chamber into the anterior chamber, leading to increased posterior chamber pressure, forward bowing of the peripheral iris, and closure of the trabecular meshwork.

What is iris bombe?

Anterior bowing (convexity) of the peripheral iris caused by pressure buildup behind the iris during pupillary block.

Why are hyperopic eyes predisposed to pupillary block?

Because they have a short axial length, thick lens, shallow anterior chamber, and crowded anterior segment.

Why does age increase the risk of pupillary block?

The lens becomes thicker and more anteriorly positioned, causing shallower anterior chamber.

At what pupil size is pupillary block maximal?

Mid-dilation (3–4.5 mm).

Why is angle closure most likely at mid-dilation?

Because iris-lens contact is maximal, the peripheral iris becomes lax, and relative pupillary block is greatest.

Which situations commonly produce mid-dilation?

Darkness, emotional stress, certain medications, and recovery after pharmacologic dilation.

Why is acute angle closure common after pharmacologic dilation rather than during full dilation?

Because during recovery, the pupil passes through mid-dilation, increasing iris-lens contact and peripheral iris laxity, maximizing relative pupillary block.

What is plateau iris?

A non-pupillary block mechanism where the ciliary body pushes the peripheral iris forward despite a relatively normal central anterior chamber depth.

What percentage of angle closure cases involve a non-pupillary block mechanism?

Up to one-third.

Is plateau iris usually associated with pupillary block?

Many patients have both mechanisms.

What happens to the iris plane in plateau iris?

It remains relatively flat.

What imaging best demonstrates plateau iris?

Ultrasound Biomicroscopy (UBM).

What classic gonioscopic sign indicates plateau iris?

Double hump sign (S-sign).

What causes the double hump sign?

The iris drapes over the anteriorly positioned ciliary body.

When is angle closure risk highest in plateau iris?

Maximum dilation.

What is the gold standard for diagnosing angle closure?

Gonioscopy.

Why is gonioscopy considered the reference standard?

It directly visualizes angle anatomy, appositional closure, PAS, and mechanism of closure.

Which imaging techniques are useful in PACG?

UBM and AS-OCT.

Why are UBM and AS-OCT useful?

They do not rely on visible light and allow visualization of structures behind the iris.

Is dark-room provocative testing still recommended?

No, it is time-consuming, misleading, and potentially dangerous.

How does PACG typically begin?

Intermittent, reversible appositional angle closure.

What converts appositional closure into permanent closure?

Formation of peripheral anterior synechiae (PAS).

Can trabecular meshwork damage become permanent even if the angle reopens?

Yes, prolonged contact may permanently damage TM function.

Why is acute PACG an ocular emergency?

Permanent blindness can occur within 2–3 days.

Typical IOP during an acute attack?

40–80 mmHg.

Classic symptoms of acute PACG?

Severe eye pain, red eye, blurred vision, colored halos, nausea, vomiting, and headache.

Classic signs of acute PACG?

Corneal edema, circumlimbal injection, fixed mid-dilated pupil, elevated IOP, and mild AC cells/flare.

Why do patients see colored halos?

Corneal edema causes diffraction of light.

Why does nausea and vomiting occur?

Vagal stimulation from markedly elevated IOP.

What pupil abnormality occurs after an acute attack?

Poorly reactive, ovoid pupil due to sphincter infarction.

What are glaukomflecken?

White-gray anterior subcapsular lens opacities caused by ischemic lens epithelial damage after acute IOP elevation.

What do glaukomflecken indicate?

Previous acute angle closure attack.

What happens to RNFL after acute PACG?

RNFL thickness decreases significantly during the first four months.

What happens to the corneal endothelium after acute PACG?

Endothelial cell count decreases.

How does intermittent PACG differ from acute PACG?

Only part of the angle closes; symptoms are mild, intermittent, and self-resolving.

Common symptoms of intermittent PACG?

Dull eye pain, blurred vision, colored halos, headache, and mild redness.

When do symptoms usually occur in intermittent PACG?

Evenings, dim lighting, movie theaters, reading, and sewing.

Why do symptoms improve during sleep?

Sleep-induced miosis and posterior movement of the lens reopen the angle.

Why are asymptomatic patients dangerous in PACG?

They may present only after severe glaucomatous damage.

Gonioscopy findings in intermittent PACG?

Irregular angle width, narrow appositional areas, and minimal PAS.

How does chronic PACG develop?

Slow progressive angle closure over months to years.

Why is chronic PACG often mistaken for POAG?

Patients usually lack symptoms and develop gradual optic nerve damage.

How is chronic PACG distinguished from POAG?

Gonioscopy.

Gonioscopy findings in chronic PACG?

Extensive appositional closure and PAS, with the superior angle commonly first affected.

What does the optic nerve appearance indicate in PACG?

Cupping proportional to the degree and duration of elevated IOP.

How can inflammatory glaucoma mimic chronic PACG?

Peripheral anterior synechiae can form after inflammation.

How do inflammatory PAS differ from PACG PAS?

Inflammatory PAS are abrupt, patchy, and non-contiguous, whereas PACG PAS are continuous and gradual.

Diseases that may produce inflammatory angle closure?

Sarcoidosis, ankylosing spondylitis, pars planitis, and juvenile rheumatoid arthritis.

Goals of treatment for PACG?

Eliminate mechanism of closure, lower IOP, and prevent optic nerve damage.

Main definitive treatments for PACG?

Laser Peripheral Iridotomy (LPI), Argon Laser Iridoplasty (ALPI), and lens extraction.

Best treatment for pupillary block?

Laser Peripheral Iridotomy (LPI).

Best treatment for plateau iris?

Argon Laser Iridoplasty (ALPI).

Why perform laser peripheral iridotomy?

Creates an alternate pathway for aqueous flow from the posterior chamber to the anterior chamber, eliminating pupillary block.

First goal during an acute attack?

Break the attack by lowering IOP before definitive laser treatment.

Medications used during acute PACG?

Topical: Timolol, Brimonidine or Apraclonidine, Dorzolamide; Systemic: Acetazolamide, Glycerol (avoid in diabetics); Miotic: Pilocarpine (only after IOP decreases).

Why is pilocarpine ineffective when IOP exceeds 40 mmHg?

The ischemic iris sphincter cannot respond to pilocarpine.

Why can pilocarpine worsen angle closure?

It may move the lens-iris diaphragm anteriorly, worsening closure.

Why should glycerol be avoided in diabetics?

It increases blood glucose.

Why should acetazolamide be used cautiously in elderly frail patients?

Higher risk of systemic adverse effects and dehydration.

What is the risk to the fellow eye if untreated?

40–80% chance of developing an acute attack within 5–10 years.