Acute Angle-Closure Glaucoma: Symptoms, Causes & Treatment

Acute angle-closure glaucoma (AACG) is a sudden and severe rise in intraocular pressure (IOP) caused by abrupt occlusion of the iridocorneal angle — the trabecular meshwork through which aqueous humor drains from the anterior chamber. When the angle closes completely, aqueous outflow stops, IOP rises rapidly (commonly to 40–80 mmHg vs. normal 10–21 mmHg), and the optic nerve sustains pressure-induced ischemic injury that can cause permanent irreversible vision loss within hours if untreated.

AACG is an ophthalmic emergency requiring same-day treatment. It presents dramatically: sudden severe unilateral eye pain, frontal headache, blurred vision with colored halos around lights, nausea and vomiting (often misdiagnosed as acute abdominal or neurological emergency), and on examination — a mid-dilated unreactive pupil, corneal edema causing haze, and a markedly elevated IOP. Unlike chronic open-angle glaucoma (which is asymptomatic), AACG's symptom severity usually drives patients to seek care urgently.

Risk factors include narrow anterior chamber angle (constitutionally predisposed in hyperopic — farsighted — eyes), female sex, Asian ethnicity (5–40× higher risk), older age (lens thickening narrows the angle progressively), and pupillary dilation from dim lighting or mydriatic drugs. Acute attacks can be precipitated by topical or systemic medications causing pupillary dilation: antihistamines, antidepressants (TCAs, SSRIs), antispasmodics, and sympathomimetics.

• Sudden severe ipsilateral eye pain — often described as deep aching pain radiating to the brow and forehead
• Sudden blurred vision — corneal edema from elevated IOP causes a 'steamy' corneal appearance
• Colored halos around lights (rainbow rings) from corneal epithelial edema
• Eye redness (conjunctival injection and ciliary flush)
• Mid-dilated non-reactive pupil — the pupillary sphincter is ischemic; the pupil appears oval and vertical
• Nausea and vomiting — prominent, often the presenting complaint leading to misdiagnosis as GI or neurological event

• Underlying narrow iridocorneal angle — the primary predisposing anatomy (hyperopic/short axial length eyes)
• Pupillary dilation triggers: dim lighting, emotional stress, topical mydriatic agents (tropicamide, phenylephrine)
• Systemic medications causing pupillary dilation or forward lens movement: antihistamines, TCAs, SSRIs, SNRIs, antispasmodics, topiramate (causes ciliary body edema — bilateral AACG), nebulized ipratropium
• Asian and South Asian ethnicity — significantly narrower anterior chamber angles
• Lens thickening with aging — narrows the angle progressively
• Precipitating factors: reading in low light, emotional upset, prone positioning

Clinical examination by an ophthalmologist: IOP measurement by tonometry (Goldmann applanation) — typically >40–80 mmHg in acute attack. Slit-lamp examination: corneal edema (hazy epithelium), shallow anterior chamber, mid-dilated oval non-reactive pupil. Gonioscopy (after IOP lowering): confirms angle closure. Optic disc assessment for glaucomatous cupping. Fellow eye gonioscopy: narrow angle warrants prophylactic treatment. Do not delay treatment waiting for imaging — this is a time-sensitive emergency.

Immediate medical IOP lowering (all simultaneously): timolol 0.5% eye drops (beta-blocker), brimonidine 0.2% (alpha-2 agonist), acetazolamide 500 mg IV or oral (carbonic anhydrase inhibitor — reduces aqueous production rapidly), pilocarpine 2% (only effective once IOP begins to fall — constricts pupil, opens angle). Systemic: IV mannitol or oral glycerol as hyperosmotic agent if IOP does not respond. Once IOP is controlled (<30 mmHg): laser peripheral iridotomy (LPI) — creates a small opening in the peripheral iris, establishing an alternative aqueous drainage pathway, permanently preventing future attacks. Prophylactic LPI in the contralateral (fellow) eye — narrow-angle fellow eyes have ~50% 5-year risk of acute attack. Surgical iridectomy if laser unavailable.

• Permanent optic nerve damage and irreversible vision loss if treatment delayed >12–24 hours
• Anterior lens opacity (glaucomflecken — subcapsular lens opacification from ischemia) visible after attack
• Fellow eye acute attack: without prophylactic LPI, 50% risk of contralateral attack within 5 years
• Chronic angle-closure glaucoma as a sequel requiring ongoing IOP management

• Angle assessment by gonioscopy in high-risk individuals (hyperopic, elderly, Asian, family history)
• Prophylactic laser peripheral iridotomy (LPI) for narrow but not yet closed angles — prevents acute attacks
• Medication review: caution with anticholinergics, antihistamines, and antidepressants in narrow-angle patients; inform prescribers of narrow-angle status
• Avoid prolonged darkness, prone positioning, and reading in dim light if known narrow-angle predisposition