Ophthalmologic emergency — sudden IOP elevation from blocked aqueous outflow; vision loss if not treated within hours.
Also known as: acute angle-closure glaucoma, AACG, angle closure crisis, pupillary block glaucoma
Overview
Sudden, marked rise in intraocular pressure (IOP) caused by mechanical obstruction of aqueous humor outflow at the trabecular meshwork from apposition of the iris against the angle. Most often results from pupillary block in an anatomically predisposed eye with a shallow anterior chamber.
Epidemiology
Incidence ~1 per 1,000 per year over age 40 in susceptible populations. Higher prevalence in Asians (especially East Asians) and Inuit; female:male approximately 3:1; mean age 55-65. Hyperopes have shallower anterior chambers and higher risk.
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Question 1EENTEasy
A 55-year-old man with diabetes presents with a painful red eye, blurred vision, and right-sided headache. He sees halos around lights and his right pupil is mid-dilated and non-reactive. Intraocular pressure (IOP) is 58 mmHg. What is the most likely diagnosis?
AAcute viral conjunctivitis
BAcute orbital cellulitis
CAcute anterior uveitis
DAcute angle-closure glaucoma
Reveal answer & full explanation
Correct answer: D — Acute angle-closure glaucoma
AAcute viral conjunctivitis
BAcute orbital cellulitis
CAcute anterior uveitis
DAcute angle-closure glaucoma✓
Why acute angle-closure glaucoma is correct
Classic features: unilateral painful red eye, blurred vision with halos around lights, fixed mid-dilated non-reactive pupil, and markedly elevated intraocular pressure (IOP) above 30-40 mmHg (58 mmHg here)
Associated symptoms include headache, nausea, and vomiting
Often precipitated by pupil dilation from dim lighting or anticholinergic medications
This is an ophthalmic emergency
Why the others are wrong
A) Acute viral conjunctivitis — does not elevate IOP or alter pupil reactivity
B) Acute orbital cellulitis — causes proptosis, pain with extraocular movement, and fever rather than halos with a fixed mid-dilated pupil and IOP of 58 mmHg
C) Acute anterior uveitis — also causes a painful photophobic red eye but with cell and flare, keratic precipitates, and a constricted pupil, with IOP typically normal or low rather than 58 mmHg
Additional high-yield points
Initial treatment: topical timolol, brimonidine, IV acetazolamide, and pilocarpine
Definitive treatment: laser peripheral iridotomy
Question 2EENTMedium
A 65-year-old female presents with sudden severe right eye pain, blurred vision, and seeing halos around lights. Eye exam shows fixed mid-dilated pupil, ciliary flush, and rock-hard globe. Intraocular pressure is 55 mm Hg. Which of the following is the most likely diagnosis?
AAcute angle-closure glaucoma
BPrimary open-angle glaucoma
CAnterior optic neuritis
DAcute anterior uveitis
Reveal answer & full explanation
Correct answer: A — Acute angle-closure glaucoma
AAcute angle-closure glaucoma✓
BPrimary open-angle glaucoma
CAnterior optic neuritis
DAcute anterior uveitis
Why Acute angle-closure glaucoma is correct
Acute angle-closure glaucoma is an ocular emergency
Anatomically narrow angle plus pupillary dilation (from dim light, anticholinergics, or sympathomimetics) causes the iris to block the trabecular meshwork, rapidly elevating intraocular pressure (IOP)
Classic symptoms: severe eye pain, blurred vision, halos around lights, headache, nausea/vomiting
Classic signs: fixed mid-dilated pupil, ciliary flush, corneal edema, rock-hard globe, IOP often 40–80 mm Hg
Definitive treatment: laser peripheral iridotomy; prophylactic iridotomy in the fellow eye
Why the others are wrong
Primary open-angle glaucoma — chronic and asymptomatic; gradual peripheral visual field loss and optic disc cupping; IOP may be mildly elevated or normal; no acute pain or fixed dilated pupil
Anterior optic neuritis — presents with pain on eye movement and an afferent pupillary defect; does not cause a rock-hard globe or markedly elevated IOP
Acute anterior uveitis — presents with a small, irregular pupil and photophobia; not associated with a fixed mid-dilated pupil or markedly elevated IOP
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Dim light (movie theater, evening) — pupil mid-dilated, maximizes iris-lens contact and iris bunching at angle
Pathophysiology
Pupillary block: in eyes with shallow anterior chamber and crowded angle, the iris contacts the anterior lens surface, blocking aqueous flow from posterior to anterior chamber. Aqueous accumulates posteriorly, bowing the iris forward (iris bombe) and pressing the peripheral iris against the trabecular meshwork. IOP rapidly rises (often >40-60 mmHg), causing optic nerve ischemia, corneal edema, and pain. Plateau iris (less common): anterior insertion of the ciliary body causes peripheral iris to crowd the angle without pupillary block.
Clinical presentation
Symptoms
Sudden severe unilateral eye pain and headache
Blurred vision and halos around lights (corneal edema)
Nausea and vomiting (vagal response) — often misdiagnosed as abdominal/GI process
Photophobia
Symptoms may follow dim-light exposure, anticholinergic use, or emotional stress
Signs / physical exam
Markedly elevated IOP — typically 40-80 mmHg (normal 10-21)
Systemic carbonic anhydrase inhibitor — acetazolamide 500 mg IV or PO (avoid in sulfa allergy with caution, sickle cell)
Topical pilocarpine 1-2% every 15 min × 2 doses once IOP is reduced below 40 mmHg (pilocarpine is ineffective at very high IOP because iris sphincter is ischemic)
Hyperosmotic agent — oral glycerol 1-2 g/kg or IV mannitol 1-2 g/kg — if IOP not responding (avoid in heart failure)
Topical corticosteroid (prednisolone acetate 1%) every 15-30 min to reduce inflammation
Second-line / adjunct
DEFINITIVE — laser peripheral iridotomy (LPI) by ophthalmology once cornea clears, usually within 24-48 hours; LPI also performed on fellow eye prophylactically (high risk)
Cataract extraction (lens-induced) increasingly favored as definitive therapy in many cases
Surgical iridectomy if LPI not feasible
Trabeculectomy or tube shunt if chronic angle closure with persistent IOP elevation
Argon laser peripheral iridoplasty in plateau iris configuration
Complications
Permanent optic nerve damage and visual field loss within hours
Central retinal artery or vein occlusion from sustained high IOP
Glaukomflecken (anterior subcapsular lens opacities from ischemia)
Iris atrophy with sphincter paralysis (fixed dilated pupil)
Chronic angle-closure glaucoma with peripheral anterior synechiae
Bilateral disease — fellow eye is at high risk; prophylactic LPI is standard
PANCE pearls
Acute angle-closure glaucoma can present with nausea and headache and be misdiagnosed as GI illness or migraine — always check the eye and the pupil.
Pilocarpine does not work when IOP is very high because the ischemic iris sphincter cannot constrict — lower IOP first with aqueous suppressants and hyperosmotics, then give pilocarpine.
Topiramate and sulfa-derivative drugs can cause idiosyncratic bilateral angle closure from ciliary body swelling — stop the drug and treat medically; iridotomy is NOT effective in this mechanism.
After medical control, definitive treatment is laser peripheral iridotomy (or lens extraction) — and the fellow eye almost always needs prophylactic iridotomy.
References
AAO 2020 — American Academy of Ophthalmology. Primary Angle Closure Disease Preferred Practice Pattern. Ophthalmology 2021;128(1):P30-P70
EAGLE Trial — Azuara-Blanco A et al. Effectiveness of early lens extraction for the treatment of primary angle-closure glaucoma (EAGLE): a randomised controlled trial. Lancet 2016;388(10052):1389-1397
ZAP Trial — He M et al. Laser peripheral iridotomy for the prevention of angle closure: a single-centre, randomised controlled trial. Lancet 2019;393(10181):1609-1618
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