Glaucoma is a group of disorders characterized by intraocular pressure (IOP) high enough to damage the optic nerve. If untreated, it leads to gradual peripheral vision loss and, ultimately, blindness.
Glaucoma occurs in several forms: chronic open-angle (primary), acute angle-closure, low tension (normal IOP that’s too high for a particular person), congenital (inherited as an autosomal recessive trait), and secondary to other causes.
Glaucoma is the second most common cause of blindness in the United States. About 2.5 million Americans are afflicted with the disease, but only 1 million know that they have it. Its incidence is highest among blacks, and it’s the single most common cause of blindness in that group. The visual prognosis is good with early treatment.
The cause of glaucoma varies according to the type of disorder:
❑ Chronic open-angle glaucoma results from overproduction of aqueous humor or from obstructed outflow of aqueous humor through the trabecular meshwork or the canal of Schlemm. This form of glaucoma frequently runs in families and affects 90% of all patients with glaucoma.
❑ Acute angle-closure (narrow-angle) glaucoma results from obstructed outflow of aqueous humor caused by anatomically narrow angles between the anterior iris and the posterior corneal surface, shallow anterior chambers, a thickened iris that causes angle closure on pupil dilation, or a bulging iris that presses on the trabeculae, closing the angle. Adhesions in the angle, referred to as peripheral anterior synechiae, may be the cause.
❑ Secondary glaucoma can result from uveitis, trauma, or drugs such as steroids. Neovascularization in the angle can result from vein occlusion or diabetes.
Clinical features vary with the form of glaucoma.
Usually bilateral, chronic open-angle glaucoma has an insidious onset and a slowly progressive course. Symptoms appear late in the disease and include mild aching in the eyes, loss of peripheral vision, seeing halos around lights, and reduced visual acuity (especially at night) that’s uncorrectable with glasses.
An ophthalmic emergency, acute angle-closure glaucoma typically has a rapid onset. Symptoms include unilateral inflammation and pain, pressure over the eye, moderate pupil dilation that’s nonreactive to light, a cloudy cornea, blurring and decreased visual acuity, photophobia, and seeing halos around lights.
Because increased IOP may induce nausea and vomiting, glaucoma may be misinterpreted as GI distress. Unless treated promptly, this acute form of glaucoma produces blindness in 3 to 5 days.
Loss of peripheral visual field, cupping of the optical disk, and increased IOP are the triad of signs that indicate glaucoma. Relevant diagnostic tests include the following:
❑ Tonometry (using an applanation, Schiøtz, or air-puff tonometer) measures IOP and provides a baseline for reference.
Normal IOP ranges between 8 and 21 mm Hg, but some patients who fall in the normal range develop signs and symptoms of glaucoma. On the other hand, some patients who have abnormally high pressure have no clinical effects.
Fingertip tension is another way to measure IOP. On gentle palpation of closed eyelids, one eye feels harder than the other in acute angle-closure glaucoma.
❑ Slit-lamp examination provides a look at the anterior structures of the eye, including the cornea, iris, and lens.
❑ Gonioscopy, by determining the angle of the anterior chamber of the eye, allows differentiation between chronic open-angle glaucoma and acute angle-closure glaucoma. The angle is normal in chronic open-angle glaucoma. In older patients, partial closure of the angle may also occur, so two forms of glaucoma may coexist.
❑ Ophthalmoscopy provides a look at the fundus, where cupping of the optic disk is visible in chronic open-angle glaucoma. This change appears later in chronic angle-closure glaucoma if the disease isn’t brought under control. A pale disk appears in acute angle-closure glaucoma.
❑ Perimetry or visual field tests help evaluate the extent of chronic open-angle deterioration by determining peripheral vision loss.
❑ Fundus photography can monitor the disk for any changes.
Drug therapy is the treatment of choice for chronic open-angle glaucoma. If this fails, argon laser trabeculoplasty or trabeculectomy is performed. Acute angle-closure glaucoma is treated with drugs, laser iridotomy, or surgical peripheral iridectomy.
For chronic open-angle glaucoma, treatment initially decreases aqueous humor production through beta-adrenergic blockers, such as timolol (contraindicated for patients with asthma or those with bradycardia) and betaxolol (a beta1-receptor antagonist); alpha agonists, such as brimonidine, to lower IOP; and topical carbonic anhydrase inhibitors such as dorzolamide.
Drug treatment also includes miotic eyedrops, such as pilocarpine, to facilitate the outflow of aqueous humor. Patients who are unresponsive to drug therapy may be candidates for iridectomy, a surgical filtering procedure that creates an opening for aqueous outflow.
Clinical tip The end stage of glaucoma may require a tube shunt or valve to keep IOP down.
In argon laser trabeculoplasty, an argon laser beam is focused on the trabecular meshwork of an open angle. This produces a thermal burn that changes the surface of the meshwork and increases the outflow of aqueous humor.
In trabeculectomy, a flap of sclera is dissected free to expose the trabecular meshwork. This discrete tissue block is then removed, and a peripheral iridectomy is performed. This procedure produces an opening for aqueous outflow under the conjunctiva, creating a filtering bleb.
Acute angle-closure glaucoma is an ocular emergency that requires immediate treatment to lower the high IOP. If the pressure doesn’t decrease with drug therapy, laser iridotomy or surgical peripheral iridectomy must be performed promptly to save the patient’s vision.
Iridectomy relieves pressure by excising part of the iris to reestablish aqueous humor outflow. A prophylactic iridectomy is performed a few days later on the patient’s other eye to prevent an acute episode of glaucoma in that eye.
Preoperative drug therapy lowers IOP with I.V. mannitol and steroid drops to quell the inflammation. Acetazolamide is used as well as pilocarpine (which constricts the pupil, forcing the iris away from the trabeculae and allowing fluid to escape) and I.V. mannitol (20%) or oral glycerin (50%) to force fluid from the eye by making the blood hypertonic. Timolol is used to decrease IOP. Severe pain may necessitate narcotic analgesics.
❑ Stress the importance of meticulous compliance with prescribed drug therapy to prevent disk changes, loss of vision, and an increase in IOP.
❑ Give the patient with acute angle-closure glaucoma medications, and prepare him physically and psychologically for laser iridotomy or surgical peripheral iridectomy.
❑ Postoperative care after laser peripheral iridectomy includes cycloplegic eyedrops (apraclonidine) to relax the ciliary muscle and decrease inflammation, thus preventing adhesions. Cycloplegics must be used only in the affected eye. The use of these drops in the normal eye may precipitate an attack of acute angle-closure glaucoma in this eye, threatening the patient’s residual vision.
❑ Encourage ambulation immediately after surgery.
❑ After surgical filtering, postoperative care includes cycloplegic dilation and topical antibiotic steroids to quell the inflammatory response to surgery.
❑ Stress the importance of glaucoma screening for early detection and prevention. All people over age 35, especially those with a family history of glaucoma, should have an annual tonometric examination.
Review other book chapters online related to Congenital glaucoma:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5 
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