Emergency Medicine Hub / HEENT & Ophthalmology • 3 min read • 2 sections

Acute Angle-Closure Glaucoma & Ocular Hypertension

Comprehensive emergency evaluation and protocolized management of Acute Angle-Closure Glaucoma (AACG): pupillary block mechanism, shallow anterior chamber anatomy, precipitating triggers (mydriatics, dim light, anticholinergics, topiramate), classic clinical presentation (severe unilateral orbital pain, nausea/vomiting, colored halos around lights, mid-dilated non-reactive pupil, 'steamy/hazy' cornea, rock-hard globe on palpation), tonometry confirming intraocular pressure (IOP > 30–50 mmHg), the 4-drug emergency IOP-lowering medical cocktail (Timolol, Apraclonidine, Prednisolone, IV Acetazolamide/IV Mannitol), Pilocarpine timing, and definitive laser peripheral iridotomy (LPI).

Resuscitation Quick Actions • First 2 Minutes

High-Acuity

Classic Presentation Triad

Severe unilateral eye pain + Colored halos around lights + Mid-dilated fixed pupil + 'Steamy' hazy cornea + Nausea/vomiting

Diagnostic IOP Cutoff

Tonopen/Tonometry confirms Intraocular Pressure > 30–40 mmHg (normal IOP is 10 to 21 mmHg; often 50–70 mmHg in acute attack)

The 4-Drug Medical Cocktail

1) Timolol 0.5% (beta-blocker), 2) Apraclonidine 1% (alpha-2 agonist), 3) Acetazolamide 500 mg IV/PO (CAI), 4) Prednisolone 1% drops

Mannitol for IOP > 50

IV Mannitol 20% (1.0 to 2.0 g/kg over 30 min); osmotically shrinks vitreous humor to pull iris away from trabecular meshwork

Pilocarpine Timing Rule

DO NOT give Pilocarpine immediately! The iris sphincter is ischemic and paralyzed at IOP > 35–40 mmHg; start pilocarpine ONLY when IOP < 30

Bilateral Laser Iridotomy

Emergent Ophthalmology consult for bilateral Laser Peripheral Iridotomy (LPI); contralateral eye is anatomically predisposed and requires prophylactic LPI

Bottom-Line Clinical Pearl

Acute Angle-Closure Glaucoma (AACG) is an ophthalmologic surgical emergency where mechanical pupillary block prevents aqueous humor from draining through the trabecular meshwork, causing Intraocular Pressure (IOP) to skyrocket from normal (10–21 mmHg) to > 40–70 mmHg, leading to irreversible optic nerve ischemia within hours. Presenting triad: SEVERE UNILATERAL PERIORBITAL PAIN WITH NAUSEA/VOMITING, 'STEAMY' CLOUDY CORNEA, and a MID-DILATED (4–6 mm) SLUGGISH OR FIXED PUPIL. Tonometry (Tonopen) confirms IOP > 30–40 mmHg. Medical resuscitation requires simultaneous administration of agents that suppress aqueous production, increase uveoscleral outflow, and osmotically dehydrate the vitreous: (1) Timolol 0.5% drops, (2) Apraclonidine 1% drops, (3) Acetazolamide 500 mg IV (or PO), and (4) IV Mannitol (1–2 g/kg) if IOP > 50 mmHg. Withhold miotic Pilocarpine 1–2% drops until IOP drops < 30 mmHg (pupillary sphincter is paralyzed by high pressure). Definitive cure is bilateral Laser Peripheral Iridotomy (LPI).

1. Pathophysiology: Relative Pupillary Block

Aqueous humor is continuously synthesized by the ciliary body epithelium in the posterior chamber, circulates through the pupil into the anterior chamber, and drains out of the eye via the trabecular meshwork and canal of Schlemm into the episcleral venous system.

In patients with anatomically predisposing shallow anterior chambers (hyperopia/farsightedness, short axial globe length, mature thick cataracts, or elderly Asian/Inuit descent), mid-dilation of the pupil (triggered by dim ambient lighting, emotional stress, sympathomimetics, or anticholinergics) brings the posterior surface of the iris into direct physical contact with the anterior lens capsule. This creates relative pupillary block, trapping aqueous humor in the posterior chamber. Fluid pressure mounts behind the iris, bowing the peripheral iris anteriorly (iris bombé) until it mechanically plasters against the trabecular meshwork, completely occluding the iridocorneal filtration angle. Intraocular pressure (IOP) spikes from a normal baseline of $10\text{ to }21\text{ mmHg}$ to $50\text{ to }80\text{ mmHg}$, occluding axoplasmic flow and microvascular perfusion to the optic nerve head.

2. Stepwise Emergency Pharmacotherapy Regimen

Medication & Class	Dosing & Route	Mechanism of Action & Vital Monitoring
Timolol 0.5% (Non-selective Beta-blocker)	1 drop topically in affected eye; can repeat in 30 min	Decreases aqueous humor production by ciliary body. Caution: can cause bronchospasm in severe asthma or bradycardia in heart block.
Apraclonidine 1% (Alpha-2 Adrenergic Agonist)	1 drop topically in affected eye	Decreases aqueous production AND increases uveoscleral outflow.
Acetazolamide (Carbonic Anhydrase Inhibitor)	500 mg IV (preferred) OR 500 mg PO	Inhibits carbonic anhydrase in ciliary processes, slashing aqueous synthesis by up to 50%. Contraindicated: severe sulfa allergy or sickle cell disease.
Prednisolone Acetate 1% (Topical Corticosteroid)	1 drop topically every 15–30 minutes	Reduces intraocular anterior chamber inflammation and ciliary spasm.
IV Mannitol 20% (Hyperosmolar Vitreous Dehydration)	1.0 to 2.0 g/kg IV infused over 30–45 minutes	Indicated if IOP > 50 mmHg or refractory to topical drops. Creates a hyperosmolar plasma gradient that pulls water out of the vitreous body, physically collapsing the vitreous and pulling the peripheral iris away from the trabecular angle.
Pilocarpine 1% to 2% (Parasympathomimetic Miotic)	1 drop topically ONLY AFTER IOP drops < 30 mmHg; repeat q15m x 2	Contracts the pupillary sphincter, pulling peripheral iris away from the iridocorneal angle (miosis). Ineffective initially because ischemia paralyzes the sphincter when $IOP > 35\text{ mmHg}$.

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