Acute angle-closure glaucoma is a sudden eye condition requiring immediate medical intervention to safeguard vision. Unlike common forms of glaucoma that progress slowly, this acute event involves the rapid buildup of pressure inside the eye. The pressure spike increases the risk of permanent vision loss with every hour lost. This condition is caused by a sudden physical obstruction within the eye’s drainage system, which must be relieved quickly to prevent irreversible damage to the optic nerve.
Recognizing the Sudden Symptoms
The onset of acute angle-closure glaucoma is abrupt, presenting with symptoms that are difficult to ignore. The most prominent sign is severe, throbbing pain in the affected eye, often intense enough to wake a person from sleep. This pain is frequently accompanied by a substantial headache, often felt around the eyebrow or forehead.
Visual disturbances occur rapidly, including significant blurring of vision and the perception of rainbow-colored rings, or halos, around lights. The eye may appear red due to congestion, and the cornea can look hazy or cloudy. These ocular symptoms are often severe enough to trigger systemic reactions.
Many individuals experience pronounced nausea and vomiting, which can sometimes lead to a misdiagnosis of a gastrointestinal or neurological problem. If any combination of severe eye pain, blurred vision, and nausea occurs, seek emergency medical care at a hospital or contact emergency services without delay. Waiting can result in irreversible blindness within a matter of hours.
Why Intraocular Pressure Spikes So Quickly
The rise in intraocular pressure (IOP) is caused by a sudden mechanical blockage of the eye’s drainage system. The eye constantly produces aqueous humor, a clear fluid that circulates within the anterior and posterior chambers and drains through the trabecular meshwork. Normal eye pressure is maintained by balancing production and outflow.
In an acute angle-closure event, the iris physically bunches up and blocks the drainage angle where the trabecular meshwork is located. The most common cause is “pupillary block,” where the lens presses against the iris, restricting aqueous humor flow between the posterior and anterior chambers. This trapped fluid forces the peripheral iris to bow forward (iris bombé), sealing off the drainage angle completely.
With the drainage pathway obstructed, aqueous humor continues to be produced but has no escape route. This trapped fluid causes the pressure inside the eye to skyrocket quickly, often reaching 40 to 80 millimeters of mercury (mm Hg), far exceeding the normal range of 10 to 21 mm Hg. This extreme pressure elevation rapidly compresses the optic nerve, leading to the severe pain and acute vision loss associated with the crisis.
Immediate Medical Interventions
Emergency treatment focuses on two goals: rapidly lowering intraocular pressure and creating a permanent solution to prevent recurrence. Medical professionals begin by administering a combination of topical and systemic medications to halt aqueous humor production and increase its outflow. Topical drops often include a beta-blocker (Timolol), an alpha-agonist (Brimonidine), and a miotic agent (Pilocarpine).
Systemic treatment is quickly initiated, typically involving an oral or intravenous carbonic anhydrase inhibitor, such as Acetazolamide, to reduce aqueous fluid secretion. If pressure remains high, an osmotic agent like intravenous Mannitol may be used to draw fluid out of the eye and into the bloodstream, reducing internal volume. These initial medications stabilize the eye and clear corneal haziness, making the definitive treatment possible.
Once eye pressure is lowered and the cornea is clear enough, the definitive treatment, laser peripheral iridotomy (LPI), is performed. LPI uses a laser to create a tiny opening in the iris that acts as a bypass. This new opening allows aqueous humor to flow freely between the posterior and anterior chambers, equalizing pressure and unblocking the natural drainage angle.
Steps After the Crisis
Following the acute attack, patients require follow-up care to manage residual damage and prevent future episodes. Even after pressure stabilization, the optic nerve must be assessed for permanent damage, which can manifest as persistent vision or visual field loss. Regular monitoring by an ophthalmologist is necessary to track recovery and ensure intraocular pressure remains controlled long-term.
A prophylactic LPI is almost always recommended for the contralateral, or unaffected, eye. Since anatomical risk factors, such as a shallow anterior chamber, are often present in both eyes, the second eye has a high risk of a similar acute attack. Performing an LPI on the second eye eliminates the pupillary block mechanism and significantly reduces the chance of a future crisis.
If significant residual vision loss has occurred, long-term management may involve additional medications or procedures to optimize the remaining vision. For some individuals, cataract surgery may be considered, as removing the natural lens—which thickens with age—can physically deepen the anterior chamber and further open the drainage angle. Post-crisis care focuses on protecting remaining vision through meticulous monitoring and proactive intervention.