acute angle-closure glaucoma

Chronic glaucoma

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Chronic glaucoma

Glaucoma is a group of eye conditions that damage the optic nerve, the health of which is vital for good vision. This damage is often caused by an abnormally high pressure in your eye.

Open-angle glaucoma

Open-angle glaucoma is the most common form of the disease. The drainage angle formed by the cornea and iris remains open, but the trabecular meshwork is partially blocked. This causes pressure in the eye to gradually increase. This pressure damages the optic nerve. It happens so slowly that you may lose vision before you’re even aware of a problem.

Angle-closure glaucoma

Angle-closure glaucoma, also called closed-angle glaucoma, occurs when the iris bulges forward to narrow or block the drainage angle formed by the cornea and iris. As a result, fluid can’t circulate through the eye and pressure increases. Some people have narrow drainage angles, putting them at increased risk of angle-closure glaucoma.

Angle-closure glaucoma may occur suddenly (acute angle-closure glaucoma) or gradually (chronic angle-closure glaucoma). Acute angle-closure glaucoma is a medical emergency.

Pigmentary glaucoma

In pigmentary glaucoma, pigment granules from your iris build up in the drainage channels, slowing or blocking fluid exiting your eye. Activities such as jogging sometimes stir up the pigment granules, depositing them on the trabecular meshwork and causing intermittent pressure elevations.

Chronic glaucoma

Chronic glaucoma is characterized by gradually progressive excavation (“cupping”) of the optic disk with loss of vision progressing from slight visual field loss to complete blindness. In chronic open-angle glaucoma, primary or secondary, intraocular pressure is elevated due to reduced drainage of aqueous fluid through the trabecular meshwork. In chronic angle-closure glaucoma, which is particularly common in Inuits and eastern Asians, flow of aqueous fluid into the anterior chamber angle is obstructed. In normal-tension glaucoma, intraocular pressure is not elevated but the same pattern of optic nerve damage occurs.

Primary (chronic) open-angle glaucoma is usually bilateral. There is an increased prevalence in first-degree relatives of affected individuals and in diabetic patients. In Afro-Caribbeans and Africans, and probably in Hispanics, it is more frequent, occurs at an earlier age, and results in more severe optic nerve damage. Secondary open-angle glaucoma may result from ocular disease, eg, pigment dispersion, pseudoexfoliation, uveitis, or trauma; or corticosteroid therapy, whether it is intraocular, topical, inhaled, intranasal or systemic.

In the United States, it is estimated that 2% of people over 40 years of age have glaucoma, affecting over 2.5 million individuals. At least 25% of cases are undetected. Over 90% of cases are of the open-angle type. Worldwide, about 45 million people have open-angle glaucoma, of whom about 4.5 million are bilaterally blind. About 4 million people, of whom approximately 50% live in China, are bilaterally blind from chronic angle-closure glaucoma

signs and symptoms

Because initially there are no symptoms, chronic glaucoma is often first suspected at a routine eye test. Diagnosis requires consistent and reproducible abnormalities in at least two of three parameters optic disk or retinal nerve fiber layer (or both), visual field, and intraocular pressure. Optic disk cupping is identified as an absolute increase or an asymmetry between the two eyes of the ratio of the diameter of the optic cup to the diameter of the whole optic disk (cup-disk ratio). (Cup-disk ratio greater than 0.5 or asymmetry between eyes of 0.2 or more is suggestive.)

Detection of optic disk cupping and associated abnormalities of the retinal nerve fiber layer is facilitated by optical coherence tomography scans. Visual field abnormalities initially develop in the paracentral region, followed by constriction of the peripheral visual field. Central vision remains good until late in the disease. The normal range of intraocular pressure is 10–21 mm Hg.

In many individuals (about 4.5 million in the United States), elevated intraocular pressure is not associated with optic disk or visual field abnormalities (ocular hypertension). Treatment to reduce intraocular pressure is justified if there is a moderate to high risk of progression to glaucoma, but monitoring for development of glaucoma is required in all cases. A significant proportion of eyes with primary open-angle glaucoma have normal intraocular pressure when it is first measured, and only repeated measurements identify the abnormally high pressure. In normal-tension glaucoma, intraocular pressure is always within the normal range

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Prevention

There are many causes of optic disk abnormalities or visual field changes that mimic glaucoma and visual field testing may prove unreliable in some patients, particularly in the older age group. Hence, the diagnosis of glaucoma is not always straightforward and screening programs need to involve ophthalmologists.

Although all persons over age 50 years may benefit from intraocular pressure measurement and optic disk examination every 3–5 years, screening for chronic openangle glaucoma should be targeted at individuals with an affected first-degree relative, at persons who have diabetes mellitus, and at older individuals with African or Hispanic ancestry. Screening may also be warranted in patients taking long-term oral or combined intranasal and inhaled corticosteroid therapy. Screening for chronic angle-closure glaucoma should be targeted at Inuits and Asians

Treatments

Prostaglandin analog eye drops are commonly used as first-line therapy because of their efficacy, lack of systemic side effects, and convenient once-daily dose (except unoprostone). All may produce conjunctival hyperemia, permanent darkening of the iris and eyebrow color, increased eyelash growth, and reduction of periorbital fat (prostaglandin-associated periorbitopathy).

Topical beta-adrenergic blocking agents may be used alone or in combination with a prostaglandin analog. They may be contraindicated in patients with reactive airway disease or heart failure. Betaxolol is theoretically safer in reactive airway disease but less effective at reducing intraocular pressure.

Brimonidine 0.2%, a selective alpha-2-agonist, and topical carbonic anhydrase inhibitors also can be used in addition to a prostaglandin analog or a beta-blocker (twice daily) or as initial therapy when prostaglandin analogs and beta-blockers are contraindicated (brimonidine twice daily, carbonic anhydrase inhibitors three times daily). All three are associated with allergic reactions. Brimonidine may cause uveitis. Apraclonidine, 0.5–1%, another alpha-2-agonist, can be used three times a day to postpone the need for surgery in patients receiving maximal medical therapy, but long-term use is limited by adverse reactions.

It is more commonly used to control acute rise in intraocular pressure, such as after laser therapy. Pilocarpine 1–4% is rarely used because of adverse effects. Oral carbonic anhydrase inhibitors (acetazolamide [Diamox], methazolamide [Neptazane], and dichlorphenamide [Daranide]) may still be used on a long-term basis if topical therapy is inadequate and surgical or laser therapy is inappropriate.

Various eye drop preparations combining two agents out of the prostaglandin analogs, beta-adrenergic blocking agents, brimonidine and topical carbonic anhydrase inhibitors are available to improve compliance when multiple medications are required. Formulations of one or two agents without preservative or not including benzalkonium chloride as the preservative are increasingly used to reduce adverse effects on the ocular surface.

Laser Therapy and Surgery

Laser trabeculoplasty is used as an adjunct to topical therapy to defer surgery and is also advocated as primary treatment. Surgery is generally undertaken when intraocular pressure is inadequately controlled by medical and laser therapy, but it may also be used as primary treatment. Trabeculectomy remains the standard procedure.

Adjunctive treatment with subconjunctival mitomycin or fluorouracil is used perioperatively or postoperatively in worse prognosis cases. Viscocanalostomy, deep sclerectomy with collagen implant and Trabectome alternative procedures that avoid a full-thickness incision into the eye are associated with fewer complications but are more difficult to perform.

In chronic angle-closure glaucoma, laser peripheral iridotomy or surgical peripheral iridectomy may be helpful. In patients with asymptomatic narrow anterior chamber angles, which includes about 10% of Chinese adults, prophylactic laser peripheral iridotomy can be performed to reduce the risk of acute and chronic angle-closure glaucoma.

However, there are concerns about the efficacy of such treatment and the risk of cataract progression and corneal decompensation. In the United States, about 1% of people over age 35 years have narrow anterior chamber angles, but acute and chronic angle-closure are sufficiently uncommon that prophylactic therapy is not generally advised.

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