Glaucoma is a set of ocular disorders often defined by increased intraocular pressures leading to optic neuropathy and vision loss if untreated. Glaucoma has traditionally been classified as open-angle or closed-angle and as primary or secondary. The angle refers to the angle between the iris and the cornea in the anterior chamber which can become structurally obstructed. By definition, primary glaucomas are not associated with known ocular or systemic disorders and usually affect both eyes. Secondary glaucomas are associated with ocular or systemic disorders and are often unilateral. Acute angle-closure glaucoma is a subset of primary angle-closure glaucoma.
The commonly accepted range for intraocular pressure is 10-22 mm Hg. Three factors affect intraocular pressure: the rate of production of aqueous humor by the ciliary body, the resistance to aqueous outflow through the trabecular meshwork and Schlemm’s canal, and the episcleral venous pressure. The normal flow of aqueous humor starts in the ciliary body, goes through the pupil and out through the trabecular meshwork and Schlemm's canal in the angle of the anterior chamber. In acute angle closure glaucoma, intraocular pressure increases rapidly due to outflow obstruction of the aqueous humor. There are several factors leading to the obstruction in acute angle closure glaucoma, but the major predisposing factor is the structural anatomy of the anterior chamber leading to a shallower angle.
Blockage of the aqueous humor occurs due to a number of predisposing anatomic variations. These variations include a shallower anterior chamber, lens size, anterior location of the iris-lens diaphragm, and a narrow entrance to the anterior chamber angle. The shallower anterior chamber angle leads to a large area of the iris and lens being in contact with each other slowing the flow of aqueous humor from the posterior chamber to the anterior chamber. This, in turn, leads to a pressure differential between the chambers called a pupillary block. The pupillary block causes bowing of the iris which narrows the angle of the anterior chamber further. This cycle will perpetuate increasing intraocular pressures leading to the clinical presentation of acute angle closure glaucoma.
There are a number of risk factors for acute angle closure glaucoma which include age, gender, race and family history.
An acute attack of angle closure glaucoma is precipitated by pupillary dilatation leading to increasing iris and lens contact increasing the pupillary block. The increasing pupillary block leads to bulging of the iris acutely closing the angle between the iris and cornea thus obstructing the aqueous humor outflow track. The intraocular pressure rises acutely leading to symptomology.
Acute angle closure glaucoma presents as a sudden onset of severe unilateral eye pain or a headache associated with blurred vision, rainbow-colored halos around bright lights, nausea, and vomiting. The physical exam will reveal a fixed midpoint pupil and a hazy or cloudy cornea with marked conjunctival injection (most prominent at the limbus). Intraocular pressure will be elevated and can be as high as 60 to 80 mm Hg in an acute attack. A mild amount of aqueous flare and cell may be seen. The optic nerve may also be swollen during an acute attack.
Measuring an elevated intraocular pressure is diagnostic. There is no need for any imaging studies. A basic metabolic panel should be checked if osmotic agents will be initiated for treatment. A gonioscopic examination by an ophthalmologist to verify angle closure makes the definitive diagnosis. Gonioscopy of the unaffected eye will reveal a narrow occludable angle given the anatomic predisposing factors to acute angle-closure glaucoma (See other issues for further discussion). Glaucomflecken (grey-white opacities on the anterior lens capsule) may be visible if previous attacks of angle-closure glaucoma have occurred.
The medical treatment for acute angle closure glaucoma aims to decrease the intraocular pressure by blocking the production of aqueous humor, increasing the outflow of aqueous humor and reducing the volume of the aqueous humor.
Initial medical therapy includes a combination of the following medications:
Intraocular pressure needs to be checked every hour.
Emergently consult ophthalmology as you begin treatment.
Definitive treatment is peripheral iridectomy after the acute episode subsides. Laser iridectomy is the treatment of choice. Surgical iridectomy is indicated when laser can not be accomplished. Iridectomy relieves the pupillary block as the pressure between the posterior and anterior chamber approaches zero by allowing the flow of aqueous humor through a different route. Iridectomy should be as peripheral as possible and covered by the eyelid to avoid monocular diplopia through this second hole in the pupil.
An untreated fellow eye has a 40-80% chance of developing an acute attack angle-closure glaucoma over 5-10 years as it shares the same anatomic predisposing factors of the first eye. Hence peripheral iridectomy should be performed in the fellow eye as well as the affected eye.
The gender and ethnicity predisposing factors to acute angle-closure glaucoma hint at a genetic predisposition to the disease in certain populations. Recent large-scale studies have shown a clear association to several genes and genetic loci with primary open-angle glaucoma, but evidence for acute angle-closure glaucoma is sparse. So far only one study has shown a genetic locus on Chromosome 11 that can cause acute angle-closure glaucoma.
Acute angle closure glaucoma is best managed by an interprofessional team that also includes an ophthalmology nurse and the pharmacist. After managing the emergency with eyedrops, the patient should be scheduled for iridectomy. Clinicians need to be aware that the other eye is also at risk for acute angle close glaucoma and prophylactic surgery is recommended.
The outcomes for patients with acute angle closure glaucoma are good after treatment, however, delay in treatment can lead to damage to the optic nerve and vision loss.
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