EENT · PANCE / PANRE

Acute Angle-Closure Glaucoma

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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Risk factors

  • Hyperopia (small anterior segment)
  • Age >50
  • Female sex
  • Asian or Inuit ancestry
  • Family history of angle closure
  • Mature cataract (thickens lens, pushes iris forward)
  • Pharmacologic mydriasis (anticholinergics, sympathomimetics, antihistamines, tricyclics, topiramate — idiosyncratic ciliary body swelling)
  • 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)
  • Conjunctival injection (ciliary flush)
  • Cloudy/steamy cornea from epithelial edema
  • Mid-dilated (4-6 mm), fixed, poorly reactive pupil
  • Shallow anterior chamber on penlight (oblique flashlight test — iris shadows nasal half)
  • Decreased visual acuity
  • Eye hard to palpation

Classic findings

Steamy cornea + mid-dilated fixed pupil + rock-hard eye with severe pain in a hyperopic older woman.

Differential diagnosis

  • Acute iritis (anterior uveitis) — Photophobia, ciliary flush, miotic pupil, cells/flare; IOP usually normal or low; topical cycloplegic + steroid
  • Conjunctivitis — Diffuse injection, no pain, clear cornea, normal pupil and IOP
  • Corneal abrasion / keratitis — Foreign body sensation, fluorescein uptake, clear pupil; topical antibiotic
  • Migraine with aura — Headache + visual symptoms; eye exam normal; responsive to migraine therapy
  • Endophthalmitis — Recent intraocular surgery or trauma, hypopyon, severe vision loss; emergent vitreous tap and inject
  • Acute hypertensive crisis / aortic dissection — Systemic symptoms; nausea + headache can mimic; check BP and ocular exam
  • Cluster headache — Unilateral periorbital pain, autonomic signs (lacrimation, miosis), normal IOP; oxygen + triptan

Diagnostic workup

Diagnostic criteria

Clinical triad: acute pain + corneal edema + IOP >30 mmHg with closed angle on gonioscopy.

Labs

  • No labs delay treatment — clinical diagnosis

Imaging

  • Goldmann or Tono-Pen IOP measurement — primary objective
  • Slit-lamp examination: shallow anterior chamber, corneal edema, mid-dilated pupil
  • Gonioscopy after IOP control — confirms closed angle, evaluates fellow eye
  • Anterior segment OCT or ultrasound biomicroscopy in equivocal cases

Diagnostic algorithm

flowchart TD
  A[Acute eye pain + headache<br/>± nausea/vomiting] --> B[Check IOP + slit lamp]
  B --> C{IOP >30 mmHg +<br/>steamy cornea +<br/>mid-dilated pupil?}
  C -->|Yes| D[AACG — emergency]
  D --> E[Call ophthalmology]
  D --> F[Topical: timolol +<br/>apraclonidine + dorzolamide]
  D --> G[Acetazolamide 500 mg<br/>IV or PO]
  G --> H{IOP <40 mmHg?}
  H -->|Yes| I[Pilocarpine 1-2%<br/>q15 min × 2]
  H -->|No| J[Mannitol IV 1-2 g/kg<br/>or oral glycerol]
  I --> K[Definitive: laser<br/>peripheral iridotomy<br/>within 24-48 h]
  J --> K
  K --> L[Prophylactic LPI<br/>on fellow eye]
  C -->|No| M[Consider iritis,<br/>conjunctivitis,<br/>keratitis, migraine]
Acute angle-closure glaucoma — emergency recognition and stepwise management.

Treatment

First-line

  • IMMEDIATE ophthalmology consult — vision is time-dependent
  • Position patient supine to allow lens to fall posteriorly
  • Topical aqueous suppressants in rapid succession (every minute × 3 then standard dosing):
  • • Topical beta-blocker — timolol 0.5%
  • • Topical alpha-2 agonist — apraclonidine 1% or brimonidine 0.2%
  • • Topical carbonic anhydrase inhibitor — dorzolamide 2% or brinzolamide 1%
  • 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.
  • Mid-dilated FIXED pupil + steamy cornea + IOP >40 mmHg = AACG until proven otherwise.
  • 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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