Acute Angle-Closure Glaucoma

Acute angle-closure glaucoma (ACG) is secondary to narrowing or closure of the anterior chamber angle, resulting in increased intraocular pressure (IOP), with subsequent damage to the optic nerve.

Pathophysiology: Normally, aqueous humor drains out of the anterior chamber via Schlemm canal in the anterior chamber angle. In ACG, this flow is impeded, and the IOP rises from a normal range of 10 to 21 mm Hg to 50 mm Hg or higher.

Clinical Presentation: ACG presents as an acutely inflamed eye. Nausea and vomiting are common and may be the presenting complaints. Eye pain and headache vary in severity. As the IOP reaches
the 50 to 60 mm Hg range, fluid is forced into the cornea, resulting in corneal edema. Patients report blurred vision and rainbow-colored halos around lights.

Acute Angle-Closure Glaucoma. The cornea is edematous, manifest by the indistinctness of the iris markings and the irregular corneal light reflex. Conjunctival hyperemia is also present.

Clinical findings include:

• tearing, 
• perilimbal injection (“ciliary flush”), 
• a cloudy (“steamy”) cornea, 
• a nonreactive mid-dilated pupil, 
• anterior chamber inflammation, and 
• an increased IOP. 
• Using a penlight or slit-lamp microscopy, the anterior chamber may appear shallow.

Management:

ACG is an emergency that requires ophthalmology consultation, and treatment is directed at reducing the IOP. Aqueous outflow is increased by topical myotics (pilocarpine) that pull the peripheral iris taut away from the anterior chamber angle.

Decreased production of aqueous is accomplished with topical β-blockers (timolol), an α-adrenergic agonist (apraclonidine), or a carbonic anhydrase inhibitor (acetazolamide or methazolamide systemically, dorzolamide topically). 

Osmotic agents reduce the aqueous volume within the eye and include glycerol, oral isosorbide, and IV mannitol. 

Latanoprost, a prostaglandin derivative, increases aqueous outflow through nontrabecular meshwork pathways.

The definitive treatment of ACG is laser peripheral iridectomy, done usually after the IOP normalizes.

Points To Remember: 

1. Vision loss and blindness can occur during the course of the attack (hours to days). ACG is a true ophthalmologic emergency.

2. Medicines with anticholinergic effects are capable of inducing pupillary dilation which might provoke an angle closure attack. These include over-the-counter decongestants, motion sickness medications, antipsychotics, and antidepressants.

3. ACG often occurs in the evening, when lower light levels cause mydriasis.

4. ACG patients may easily be misdiagnosed initially as having a migraine headache or a CNS catastrophe because they may present with severe headache and vomiting.

5. The elevated IOP in acute ACG can be reduced pharmacologically by three mechanisms: first, by opening the closed angle with myotics; second, by reducing aqueous formation with β-blockers, α-agonists, or carbonic anhydrase inhibitors; and third, by reducing the aqueous volume within the eye by osmotic agents.