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Angle-Closure Glaucoma

Clinical Presentation

Acute angle-closure glaucoma presents as a sudden, painful red eye with decreased vision and a fixed, mid-dilated pupil that will not react to light. It is an ophthalmic emergency. The pupil finding is not incidental: pressure-induced ischemia of the iris sphincter muscle paralyzes it in that position. Halos around lights often accompany the pain, produced when acutely elevated IOP causes corneal edema and the waterlogged stroma scatters incoming light. Primary open-angle glaucoma almost never produces this symptom, which makes halos a useful bedside discriminator between the two conditions.

Chronic angle-closure glaucoma looks nothing like this. Instead of one dramatic attack, repeated and prolonged episodes of iridotrabecular contact gradually scar the angle, laying down peripheral anterior synechiae that permanently seal off sections of the trabecular meshwork. Most patients feel nothing as this happens, so the pressure climbs for months or years before anyone notices. By the time vision loss or an incidental high reading brings the patient in, optic nerve damage can already be advanced, which is why clinicians sometimes call it "creeping" glaucoma.

Risk Factors

Hyperopia is the key anatomic risk factor. A hyperopic eye is shorter along its axial length, which crowds the anterior segment and leaves a shallow anterior chamber. That anatomy sets up pupillary block: the iris and lens sit close enough together that aqueous cannot pass easily from the posterior chamber to the anterior chamber through the pupil. Pressure builds behind the iris and bows it forward into the angle, narrowing or closing it. The risk profile is close to a mirror image of POAG, which tracks instead with myopia, thin corneas, and African ancestry.

Management

Acute management has two parts. Pharmacologic treatment starts with pilocarpine, a miotic that contracts the sphincter pupillae and pulls the peripheral iris away from the trabecular meshwork, mechanically opening the angle. The definitive treatment is a laser peripheral iridotomy (LPI), which uses a YAG laser to create a permanent hole in the peripheral iris. That hole equalizes pressure between the posterior and anterior chambers so pupillary block cannot recur. LPI treats the acute attack and is also used prophylactically, either in the fellow eye or in patients with anatomically narrow but not yet closed angles.

Common Pitfall: Malignant (Ciliary Block) Glaucoma

Malignant glaucoma looks similar at first glance: a flat anterior chamber and high IOP. The mechanism, though, is entirely different. Aqueous is misdirected posteriorly into the vitreous cavity instead of flowing forward, raising vitreous pressure and pushing the entire lens-iris diaphragm anteriorly. This flattens both the central and peripheral anterior chamber despite a patent iridotomy. That combination, a flat chamber with a working iridotomy already in place, is exactly what should raise suspicion, since ordinary pupillary block resolves once the LPI is functioning.

High-Yield Pearls

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