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Glaucoma is a disease of elevated intraocular pressure leading to optic nerve cupping and visual field loss. Elevated intraocular pressure is defined as a pressure greater than 21 mm Hg and may occur in as much as 15 percent of the elderly population. Glaucoma is difficult to define and diagnose precisely because modestly elevated pressures may never cause glaucomatous damage.

The essential pathophysiologic feature of glaucoma is an intraocular pressure that is too high for the optic nerve. The exact mechanism of optic nerve damage has not been established and is probably a combination of factors. Increased intraocular pressure increases vascular resistance, causing decreased vascular perfusion of the optic nerve and ischemia. The increased pressure can interfere with axoplasmic flow in the ganglion cell axons, causing cell dysfunction and death; and it can compress the lamina cribrosa, the sieve-like structure through which axons pass when leaving the eye. The altered supporting structure may then interfere with axonal function. These different mechanisms of axonal damage are of variable importance in different patients, but the final result is loss of ganglion cells and their axons, increased optic nerve cupping, and glaucoma.

The pathophysiology of increased intraocular pressure can best be understood in terms of the anatomy and physiology of aqueous flow. The iris divides the front of the eye into anterior and posterior chambers that communicate through the pupil. Aqueous humor is produced by the ciliary body, fills the posterior chamber, flows through the pupil into the anterior chamber.

Acute angle-closure glaucoma presents with a painful red eye. The physical findings include decreased visual acuity, redness, fixed and unreactive pupil in mid-dilation, and corneal haziness. Occasionally, the principal symptoms are nausea and vomiting.

Chronic Open-Angle Glaucoma

The objective of treatment is stabilization of the intraocular pressure in a range that will prevent optic nerve damage and visual field loss. Therapy involves medications that reduce aqueous production.


Pilocarpine, the most frequently used parasympathomimetic, acts by contracting the ciliary body.


act to increase endogenous cholinergic effects and are used to treat patients in whom pilocarpine is inadequate or who prefer the less frequent dosage.


Epinephrine is a sympathomimetic drug that decreases aqueous production and may increase aqueous outflow. It is additive in effect to pilocarpine and may be used in combination. The ocular side effects of epinephrine include a burning sensation, conjunctival pigmentation, conjunctival hyperemia, and allergic reactions. Many topical side effects may be reduced by using dipivefrin hydrochloride (Propine).


decrease aqueous humor production when applied topically and, because they have fewer ocular side effects than pilocarpine and need only twice-daily administration, they have become important first-line.

Carbonic anhydrase inhibitors,

such as acetazolamide, reduce aqueous production and are used when topical medications do not adequately lower intraocular pressure. They are usually used in combination with and are additive.

Sequence of Medical Therapy.

Most patients are treated first with a topical beta-blocker, then with epinephrine, pilocarpine, anticholinesterases, and finally carbonic anhydrase inhibitors.

Laser and Surgical Therapies.

Laser trabeculoplasty effectively lowers intraocular pressure in many patients inadequately controlled by medical therapy. The argon laser is used to place approximately one hundred 50-m spots circumferentially on the trabecular meshwork. Its effectiveness appears to be due to a "tightening."

Surgical intervention should be considered when maximal medical therapy and laser trabeculoplasty.

Acute Angle-Closure Glaucoma

This condition requires prompt recognition and treatment with a miotic agent such as pilocarpine, followed by urgent referral to the ophthalmologist. Pilocarpine is given as one drop of the 4% solution in the involved eye every 20 minutes. Then acetazolamide, 250 mg, is given by mouth or 500 mg intravenously, and the patient is taken to the ophthalmologist.


Drugs that increase intraocular pressure should be used cautiously. These include systemic and topical steroids, particularly when applied to the eye. Drugs with anticholinergic effects may precipitate

Most patients are treated first with topical beta-adrenergic antagonists, then with epinephrine, pilocarpine, an anticholinesterase, and finally a carbonic anhydrase inhibitor.