Angle-closure glaucoma is glaucoma associated with a physically obstructed anterior chamber angle, which may be chronic or, rarely, acute. Symptoms of acute angle closure are severe ocular pain and redness, decreased vision, colored halos around lights, headache, nausea, and vomiting. Intraocular pressure (IOP) is elevated. Immediate treatment of the acute condition with multiple topical and systemic drugs is required to prevent permanent vision loss, followed by the definitive treatment, iridotomy.
Angle-closure glaucoma accounts for about 10% of all glaucomas in the US.
Angle-closure glaucoma is caused by factors that either pull or push the iris up into the angle (ie, junction of the iris and cornea at the periphery of the anterior chamber), physically blocking drainage of aqueous and raising IOP (see Table 2: Glaucoma: Angle-Closure Glaucoma: Classification Based on Mechanisms of Outflow Obstruction*). Elevated IOP damages the optic nerve.
Angle closure may be primary (cause is unknown) or secondary to another condition (see Table 1: Glaucoma: Open-Angle Glaucoma: Classification Based on Mechanisms of Outflow Obstruction*) and can be acute, subacute (intermittent), or chronic.
Primary angle-closure glaucoma:
Narrow angles are not present in young people. As people age, the lens of the eye continues to grow. In some but not all people, this growth pushes the iris forward, narrowing the angle. Risk factors for developing narrow angles include family history, advanced age, and ethnicity; risk is higher among people of Asian and Inuit ethnicity and lower among people of European and African ethnicity.
In people with narrow angles, the distance between the pupillary iris and the lens is also very narrow. When the iris dilates, forces pull it centripetally and posteriorly causing iris–lens contact, which prevents aqueous from passing between the lens and iris into the anterior chamber (this mechanism is termed pupillary block). Pressure from the continued secretion of aqueous into the posterior chamber by the ciliary body pushes the peripheral iris anteriorly (causing a forward-bowing iris called iris bombe), closing the angle. This closure blocks aqueous outflow, resulting in rapid (within hours) and severe (> 40 mm Hg) elevation of IOP. Because of the rapid onset, this condition is called primary acute angle-closure glaucoma and is an ophthalmic emergency requiring immediate treatment. Non-pupillary block mechanisms include plateau iris syndrome in which the central anterior chamber is deep, but the peripheral anterior chamber is made shallow by a ciliary body that is displaced forward.
Intermittent angle-closure glaucoma occurs if the episode of pupillary block resolves spontaneously after several hours, usually after sleeping supine.
Chronic angle-closure glaucoma occurs if the angle narrows slowly, allowing scarring between the peripheral iris and trabecular meshwork; IOP elevation is slow.
Pupillary dilation (mydriasis) can push the iris into the angle and precipitate acute angle-closure glaucoma in any person with narrow angles. This development is of particular concern when applying topical agents to dilate the eye for examination (eg, cyclopentolate, phenylephrine) or for treatment (eg, homatropine) or when giving systemic drugs that have the potential to dilate the pupils (eg, scopolamine, α-adrenergic agonists commonly used to treat urinary incontinence, drugs with anticholinergic effects).
Secondary angle-closure glaucomas:
The mechanical obstruction of the angle is due to a coexisting condition, such as proliferative diabetic retinopathy (PDR), ischemic central vein occlusion, uveitis, or epithelial down-growth. Contraction of a neovascular membrane (eg, in PDR) or inflammatory scarring can pull the iris into the angle.
Symptoms and Signs
Acute angle-closure glaucoma:
Patients have severe ocular pain and redness, decreased vision, colored halos around lights, headache, nausea, and vomiting. The systemic complaints may be so severe that patients are misdiagnosed as having a neurologic or GI problem. Examination typically reveals conjunctival hyperemia, a hazy cornea, a fixed mid-dilated pupil, and anterior chamber inflammation. Vision is decreased. IOP is usually 40 to 80 mm Hg. The optic nerve is difficult to visualize because of corneal edema, and visual field testing is not done because of discomfort.
Chronic angle-closure glaucoma:
This type of glaucoma manifests similarly to open-angle glaucoma (see Glaucoma: Primary Open-Angle Glaucoma). Some patients have ocular redness, discomfort, blurred vision, or headache that lessens with sleep (perhaps because of sleep-induced miosis and posterior displacement of the lens by gravity). On gonioscopy, the angle is narrow, and peripheral anterior synechiae (PAS) may be seen. IOP may be normal but is usually higher in the affected eye.
Diagnosis of acute angle-closure glaucoma is clinical and by measurement of IOP. Gonioscopy may be difficult to do in the involved eye because of a clouded cornea with friable corneal epithelium. However, examination of the other eye reveals a narrow or occludable angle. If the other eye has a wide angle, a diagnosis other than primary angle-closure glaucoma should be considered.
Diagnosis of chronic angle-closure glaucoma is based on the presence of PAS on gonioscopy and characteristic optic nerve and visual field changes (see Glaucoma: Symptoms and Signs).
Acute angle-closure glaucoma:
Treatment must be initiated immediately because vision can be lost quickly and permanently. The patient should receive several drugs at once. A suggested regimen is timolol 0.5% one drop q 30 min for 2 doses; pilocarpine 2 to 4% one drop q 15 min for the first 1 to 2 h; apraclonidine 0.5 to 1% one drop q 30 min for 2 doses; acetazolamide 500 mg po initially (IV if patients are nauseated) followed by 250 mg q 6 h; and an osmotic agent, such as oral glycerol 1 mL/kg diluted with an equal amount of cold water, mannitol 1.0 to 1.5 mg/kg IV, or isosorbide 100 g po (220 mL of a 45% solution). (Note: This form of isosorbide is not isosorbide dinitrate.) Response is evaluated by measuring IOP. Miotics are generally not effective when IOP is > 40 or 50 mm Hg because of an anoxic pupillary sphincter.
Definitive treatment is with laser peripheral iridotomy (LPI), which opens another pathway for fluid to pass from the posterior to the anterior chamber, breaking the pupillary block. It is done as soon as the cornea is clear and inflammation has subsided. In some cases the cornea clears within hours of lowering the IOP; in other cases, it can take 1 to 2 days. Because the chance of having an acute attack in the other eye is 80%, LPI is done on both eyes.
The risk of complications with LPI is extremely low compared with its benefits. Glare, which can be bothersome, may occur if the iridotomy is not placed superiorly enough for the upper eyelid to cover it.
Chronic angle-closure glaucoma:
Patients with chronic, subacute, or intermittent angle-closure glaucoma should also have LPI. Additionally, patients with a narrow angle, even in the absence of symptoms, should undergo prompt LPI to prevent angle-closure glaucoma.
The drug and surgical treatments are the same as with open-angle glaucoma. Laser trabeculoplasty is relatively contraindicated if the angle is so narrow that additional PAS may form after the laser procedure. Typically, partial-thickness procedures are not indicated.
Last full review/revision May 2013 by Douglas J. Rhee, MD
Content last modified May 2013