Acute angle-closure 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 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, 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.
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.
Acute angle-closure glaucoma
Acute angle-closure glaucoma occurs when the flow of aqueous humour out of the eye is blocked and pressure inside the eye becomes too high very quickly. It is an emergency because if it is not treated quickly, it can lead to permanent loss of vision. Acute angle-closure glaucoma is also sometimes referred to as acute closed-angle glaucoma or just acute glaucoma.
Primary acute angle-closure glaucoma (acute angle-closure crisis) results from closure of a preexisting narrow anterior chamber angle. The predisposing factors are shallow anterior chamber, which may be associated with farsightedness or short stature (or both); enlargement of the crystalline lens with age; and inheritance, such as among Inuits and Asians.
Closure of the angle is precipitated by pupillary dilation and thus can occur from sitting in a darkened theater, during times of stress, following nonocular administration of anticholinergic or sympathomimetic agents (eg, nebulized bronchodilators, atropine for preoperative medication, antidepressants, bowel or bladder antispasmodics, nasal decongestants, or tocolytics) or, rarely, from pharmacologic mydriasis.
Subacute primary angle-closure glaucoma may present as recurrent headache. Secondary acute angle-closure glaucoma, which does not require a preexisting narrow angle, may occur in anterior uveitis, dislocation of the lens, or due to various drugs. Symptoms are the same as in primary acute angle-closure glaucoma, but differentiation is important because of differences in management. Acute glaucoma, for which the mechanism may not be the same in all cases, can occur in association with hemodialysis. (Chronic angle-closure glaucoma presents in the same way as chronic open-angle glaucoma.)
Patients with acute glaucoma usually seek treatment immediately because of extreme pain and blurred vision, though there are subacute cases. Typically, the blurred vision is associated with halos around lights. Nausea and abdominal pain may occur. The eye is red, the cornea cloudy, and the pupil moderately dilated and nonreactive to light. Intraocular pressure is usually over 50 mm Hg, producing a hard eye on palpation
Initial treatment is reduction of intraocular pressure. A single 500-mg intravenous dose of acetazolamide, followed by 250 mg orally four times a day, together with topical medications is usually sufficient. Osmotic diuretics, such as oral glycerin and intravenous urea or mannitol—the dosage of all three being 1–2 g/kg—may be necessary if there is no response to acetazolamide.
In primary acute angle-closure glaucoma, once the intraocular pressure has started to fall, topical 4% pilocarpine, 1 drop every 15 minutes for 1 hour and then four times a day, is used to reverse the underlying angle closure. The definitive treatment is laser peripheral iridotomy (Figure 7–1)
or surgical peripheral iridectomy. Cataract extraction is a possible alternative. If it is not possible to control the intraocular pressure medically, the angle closure may be overcome by corneal indentation, laser treatment (argon laser peripheral iridoplasty), cyclodiode laser treatment, or paracentesis; or by glaucoma drainage surgery as for uncontrolled open-angle glaucoma.
All patients with primary acute angle-closure should undergo prophylactic laser peripheral iridotomy to the unaffected eye, unless that eye has already undergone cataract or glaucoma surgery. Whether prophylactic laser peripheral iridotomy should be undertaken in asymptomatic patients with narrow anterior chamber angles is mainly influenced by the risk of the more common chronic angle-closure.
Untreated acute angle-closure glaucoma results in severe and permanent visual loss within 2–5 days after onset of symptoms. Affected patients need to be monitored for development of chronic glaucoma.