angle-closure glaucoma

**Pathophysiology** - Aqueous humor is produced by the ciliary body epithelium (nonpigmented), flows from the posterior chamber through the pupil into the anterior chamber, and drains via the trabecular meshwork into Schlemm canal (conventional pathway). A minor portion drains via the uveoscleral pathway. - In angle-closure glaucoma, the peripheral iris apposes the trabecular meshwork, obstructing outflow. The most common mechanism is relative pupillary block: the iris–lens contact impedes aqueous flow from the posterior to the anterior chamber, so pressure builds behind the iris and pushes it forward (iris bombé), closing the angle. - Result: abrupt IOP rise (often 40–80+ mmHg; normal 10–21), which causes corneal edema (halos, hazy cornea), ischemia of the optic nerve head, and retinal ganglion cell death. Permanent vision loss can occur within hours to days if untreated.

**Risk factors** - Hyperopia (farsightedness) with a short axial length and shallow anterior chamber - Older age (lens thickens with age, narrowing the angle) - Female sex - Asian (especially East Asian) and Inuit ancestry - Family history - Precipitants include dim light or mydriasis (pupil dilation makes the iris thicker and more likely to block the angle). Examples are a dark room or movie theater, stress, anticholinergics (atropine, scopolamine, tropicamide drops), sympathomimetics (phenylephrine), TCAs, antihistamines, and topiramate (can cause bilateral ciliary effusion and secondary angle closure).

**Clinical presentation (acute)** - Severe unilateral eye pain and headache - Blurred vision and halos around lights - Nausea and vomiting (may mimic an abdominal or neurologic emergency) - Conjunctival injection (ciliary flush) - Cloudy, edematous cornea - Mid-dilated, nonreactive (fixed) pupil - A rock-hard globe on palpation - Shallow anterior chamber

Subacute or intermittent attacks cause transient halos and mild pain, which resolve when the pupil constricts (for example, in light or with sleep).

**Diagnosis** - Clinical diagnosis supported by tonometry (elevated IOP). - Gonioscopy shows a closed angle. Do not perform it first in an acute attack with a hazy cornea. Anterior segment OCT or ultrasound biomicroscopy can also be used. - Fundus: optic disc cupping develops with chronic or repeated damage.

**Management** 1. Emergent ophthalmology consult. 2. Medical lowering of IOP: - Topical β-blocker (timolol), which decreases aqueous production - α2-agonist (apraclonidine, brimonidine), which decreases aqueous production - Topical or systemic carbonic anhydrase inhibitor (dorzolamide, acetazolamide), which decreases aqueous production - Topical corticosteroid (prednisolone) to reduce inflammation - Pilocarpine, which causes miosis and pulls the iris away from the angle. It works only once IOP has fallen enough for the sphincter to respond (it is ineffective at very high IOP because of iris ischemia). - Hyperosmotic agents (IV mannitol, oral glycerol) if refractory 3. Definitive treatment: laser peripheral iridotomy (creates a hole in the peripheral iris so aqueous bypasses the pupil). Prophylactic iridotomy is also done on the fellow eye, which is at high risk. Lens extraction is an option as well.

**Avoid** - Mydriatics and anticholinergics - Do not use prostaglandin analogs (latanoprost) as first-line in acute attacks, as they are less useful and inflammation may worsen the picture. Consider them an adjunct only.

**Contrast with open-angle glaucoma** - Open-angle (POAG) is more common (especially in African American patients and the elderly). The angle is open, with reduced outflow through the trabecular meshwork. It is insidious, painless, and bilateral, with peripheral vision loss first ("tunnel vision") and increased cup-to-disc ratio. - Angle-closure is acute, painful, and typically unilateral, and is an emergency.

**High-yield board pearls** - Classic vignette: an older woman, hyperopic, who develops severe eye pain, headache, halos, and vomiting after a movie theater visit or after dilating drops or anticholinergic or sympathomimetic drugs. - Mid-dilated fixed pupil + hazy cornea + red eye = angle closure. - Beware the mimic: vomiting and headache can lead to a wrong GI or neurologic diagnosis. - Drug classes to remember: miotics (pilocarpine) open the angle in angle-closure. Mydriatics worsen it. - Other causes of secondary angle closure: neovascularization (diabetic retinopathy, central retinal vein occlusion), uveitis with posterior synechiae, lens subluxation, and tumors.