Glaucoma is a group of disorders characterized by an abnormally high intraocular pressure (IOP), which can damage the optic nerve. If untreated, it can lead to gradual peripheral vision loss and, ultimately, blindness. (See Blindness.) Glaucoma occurs in several forms: chronic open-angle (primary), acute angle-closure, congenital (inherited as an autosomal recessive trait), and secondary to other causes. The prognosis for maintaining vision is good with early treatment.
Chronic open-angle glaucoma results from overproduction of aqueous humor or obstruction to its outflow through the trabecular meshwork or the canal of Schlemm. (See Normal flow of aqueous humor, page 1184.) This form of glaucoma, which is estimated to be present in 1% to 2% of people older than age 40, is frequently familial in origin and affects 90% of all patients with glaucoma. Diabetes and systemic hypertension have also been associated with this form of glaucoma.
Acute angle-closure (narrow-angle) glaucoma results from obstruction to the outflow of aqueous humor due to 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 (peripheral anterior synechiae).
Blacks are four times more likely to have this disorder than whites, and people with a family history of open-angle glaucoma are twice as likely to develop it than people without a family history of this disorder. The use of systemic anticholinergic medications, such as atropine or eye dilation drops, in a person who’s already at high-risk for acute glaucoma increases the risk. Other risk factors include farsightedness and age-related changes that create an increase in intraocular pressure.
Congenital glaucoma occurs when there is an abnormal fluid drainage angle of the eye. It may be caused by congenital infections such as TORCH virus (toxoplasmosis, other [varicella, mumps, parvovirus, human immunodeficiency virus], rubella, cytomegalovirus, and herpes), Sturge-Weber syndrome, or retinopathy of prematurity.
Secondary glaucoma can result from uveitis, trauma, or drugs (such as steroids). Neovascularization in the angle can result from vein occlusion or diabetes.
Chronic open-angle glaucoma is usually bilateral, with 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 isn’t correctable with glasses.
Acute angle-closure glaucoma typically has a rapid onset, constituting an ophthalmic emergency. Symptoms include acute pain in a unilaterally inflamed eye, with 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. Increased IOP may induce nausea and vomiting, which may cause glaucoma to be misinterpreted as GI distress. Unless treated promptly, this acute form of glaucoma produces blindness in 3 to 5 days.
❑ testing IOP
❑ measuring the visual field and noting changes, such as an enlarged blind spot and loss of peripheral vision field
❑ observing changes in the cup/disk ratio of the optic nerve head.
Relevant diagnostic tests include:
❑ Tonometry (using an applanation tonopen or air puff tonometer) — This test measures the IOP and provides a baseline for reference. Normal IOP ranges from 8 to 21 mm Hg. However, patients who fall within this normal range can develop signs and symptoms of glaucoma, and patients who have abnormally high pressure may 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 — The slit lamp facilitates examination of the anterior structures of the eye: the cornea, iris, and lens.
❑ Gonioscopy — By determining the angle of the anterior chamber of the eye, this test enables differentiation between chronic open-angle glaucoma and acute angle-closure glaucoma. The angle is normal in chronic open-angle glaucoma. However, in older patients, partial closure of the angle may occur, so that two forms of glaucoma may co-exist.
❑ Ophthalmoscopy — This test enables the examiner to look at the fundus to establish if there are any cup/disk ratio changes. (See Optic disk changes.) These changes appear later in chronic glaucoma if the disease isn’t brought under control.
❑ Fundus photography — Pictures of the optic nerve head are made to track changes.
❑ Perimetry or visual field tests — These reveal the extent of damage to the optic neurons, signaled by an enlarged blind spot and loss of peripheral vision.
For chronic open-angle glaucoma, treatment initially decreases IOP through the use of an alpha antagonist, brimonidine tartrate (Alphagan), and then beta blockers, such as timolol (contraindicated for asthmatics or patients with bradycardia) or betaxolol (Betoptic) to reduce aqueous humor production. A topical anhydrase inhibitor is used in preference to a systemic anhydrase inhibitor such as acetazolamide. A tubo-plast or tube shunt or valve may also be used. Miotic eyedrops such as pilocarpine facilitate the outflow of aqueous humor.
Patients who are unresponsive to drug therapy may be candidates for argon laser trabeculoplasty (ALT) or a surgical filtering procedure called trabeculectomy, which creates an opening for aqueous outflow. In ALT, 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. Then this discrete tissue block is removed and a peripheral iridectomy is performed. This produces an opening for aqueous outflow under the conjunctiva, creating a filtering bleb. In chronic refractory glaucoma, a tubo-plast or tube shunt or valve is used to keep IOP within normal limits.
Acute angle-closure glaucoma is an ocular emergency requiring immediate treatment to lower the high IOP. Preoperative drug therapy lowers IOP with I.V. acetazolamide, pilocarpine (constricts the pupil, forcing the iris away from the trabeculae, allowing fluid to escape), timolol, and a topical steroid to quiet the inflammatory response, along with I.V. mannitol (20%) or oral glycerin (50%) to force fluid from the eye by making the blood hypertonic. Latanoprost is a topical medication that helps drain the aqueous outflow from the eye and lower the IOP. Oral medication or topical drops may be prescribed separately or in combination. Severe pain may necessitate administration of opioid analgesics. If 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 other eye to prevent an acute episode of glaucoma in the normal eye.
❑ Stress the importance of meticulous compliance with prescribed drug therapy to prevent an increase in IOP, resulting in disk changes and loss of vision.
❑ For the patient with acute angle-closure glaucoma, give medications as ordered, and prepare him physically and psychologically for laser iridotomy or surgery.
❑ Postoperative care after peripheral iridectomy includes cycloplegic eyedrops to relax the ciliary muscle and to decrease inflammation, thus preventing adhesions.
❑ Encourage ambulation immediately after surgery.
❑ Following surgical filtering, postoperative care includes dilation and topical steroids to rest the pupil.
❑ Stress the importance of glaucoma screening for early detection and prevention. All people older than age 35, especially those with family histories 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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Title: Professional Guide to Diseases (Eighth Edition)
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2005
ISBN: 1-58255-370-X
» Next page: Glaucoma (Handbook of Diseases)
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