creation date: 2026-06-16 19:25
tags: Pathologies
Angle-Closure Glaucoma
Background
Definitions
Angle-closure glaucoma is a type of glaucoma characterized by a narrowing or closure of the anterior chamber angle.
Glaucomas are optic neuropathies that involves the atrophy of the optic nerve head and is associated with increased intraocular pressure.
Primary angle-closure: anatomic predisposition to this type of glaucoma
Secondary angle-closure: secondary process narrows or closes the anterior chamber
Risk Factors
Glaucoma is the second leading cause of blindness worldwide (behind cataracts). Risk factors include:
- Family history of angle-closure glaucoma
- Age >60
- Female sex
- Hyperopia
- Certain medications
- Pseudoexfoliation
- Inuit and East Asian descent (in contrast, open-angle glaucoma is a more common in White and Black populations)
Pathogenesis
In normal physiology, aqueous humour is produced by the ciliary body, flows through the pupil, and exits the eye through the anterior chamber angle. The balance of fluid production and drainage determines intraocular pressure (IOP).
Primary angle-closure
In primary angle-closure, the lens is anatomically too far forward and rests against the iris. This blocks the pupil, causing pressure build up behind the iris. This pressure causes the peripheral iris to bow forward and cover all/part of the anterior chamber angle.
Prolonged or repeated iris-angle contact damages the trabecular meshwork and further impairs drainage. The build up of IOP damages the optic nerve causing either:
- Acute angle-closure: entire angle blocked suddenly leading to acute symptoms
- Chronic angle-closure: only portion of angle blocked but scarring develops causing progressive damage
Secondary angle-closure
A number of conditions can deform the iris so that it is retracted into the angle (pulling) or push the iris/ciliary body into the angle (pushing).
Pulling conditions:
- Inflammation or blood in angle causing fibrosis and contraction (uveitis, hyphema)
- Neovascularization of iris (poorly controlled diabetes, retinal artery or vein occlusion)
- Abnormal corneal endothelial cell proliferation
- Prolonged shallowing of anterior chamber resulting in iris-angle contact due to trauma or surgery
- Epithelial cell or fibroblast invasion
Pushing conditions:
- Fibrosis of pupil to anterior surface of lens
- Choroidal swelling or hemorrhage (due to procedures or drug reactions)
- Plateau iris syndrome (developmental anomaly)
- Large or anteriorly displaced lens
- Aqueous misdirection (fills vitreous cavity instead, likely due to surgery)
- Choroidal hemorrhage or effusion
- Space-occupying lesion in posterior segment of eyeball
- Developmental syndromes causing fibrosis in posterior of eyeball
Clinical Presentation
Signs & Symptoms
The rapidity and degree of IOP elevation determines whether symptoms occur.
Common symptoms of rapid rise in IOP are:
- Decreased vision
- Halos around lights
- Headache
- Severe eye pain
- Nausea and vomiting
Signs include:
- Conjunctival redness
- Corneal edema or cloudiness (appears hazy with no stain)
- Shallow anterior chamber
- Mid-dilated pupil (4-6 mm) with poor light reactivity
Findings may occur in evening when lower light levels causes mydriasis (pupil dilation) and that blocks narrow angle.
Note that chronic angle-closure glaucoma may be asymptomatic due to slower rise in IOP.
History & Physical Exam
Diagnosis
Criteria
Diagnosis is made by an ophthalmologist using complete ophthalmic examination. The definitive diagnosis is made with gonioscopy which allows for visualization of the angle.
Work-up
Differential
Primary differential are those that also cause red eye.
These are generally differentiated with the signs and symptoms but not all cases of angle-closure glaucoma show classic manifestations.
Red Flags / Complications
Late or untreated angle-closure glaucoma can result in irreversible damage to the optic nerve within hours.
Management
Management consist of control of IOP followed by reversal of the angle-closure with laser peripheral iridotomy (or other surgical management).
Management is via ophthalmologist.
Emergency Empiric Therapy
In the case where an ophthalmologist is not available for ≥1 hour and the suspicion of acute attack is high, medical therapy may need to be initiated.
If vision is normal, treatment should only be initiated if IOP is significantly elevated (>40 mmHg).
Example regimen would be one drop of each of the following:
- 0.5% timolol maleate
- 1% apraclonidine
- 2% pilocarpine