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Glaucoma is characterized by progressive visual field loss caused by nerve damage from increased intraocular pressure.

A. Open-angle glaucoma is the most common form of glaucoma and is caused by a malfunction of the trabecular meshwork despite normal angle structures by gonioscopic examination. It is asymptomatic, and the etiology is multifactorial. Risk factors associated with an increased tendency toward the development of open-angle glaucoma include a family history of the disease, age, black race, diabetes, hypertension, and myopia. Treatment includes topical cholinergic or adrenergic agonists, b-adrenergic antagonists, topical carbonic anhydrase inhibitors (brinzolamide, dorzolamide), and topical prostaglandin inhibitors (latanoprost). Systemic carbonic anhydrase inhibitors can be added if topical agents do not reduce intraocular pressure adequately.

B. Angle-closure glaucoma results from obstruction of the outflow of aqueous humor through the trabecular meshwork. Common signs include conjunctival hyperemia, corneal edema, and a fixed middilated pupil. An acute rise in pressure may result in pupil dilatation; eye or face pain, or both; nausea; vomiting; loss of visual acuity; and/or seeing colored halos around lights. An acute angle-closure attack should be treated promptly in coordination with an ophthalmologist. Therapeutic agents include acetazolamide, 250 mg PO or IV; 0.05% timolol, 1 gtt bid; and 0.5% apraclonidine, 1 gtt bid, in addition to other topicals. Ophthalmologic referral for mild cases is necessary within 12 hours.

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