Glaucoma

Glaucoma is responsible for at least 10% of people with blindness in the United States. Glaucoma is four times more common in African Americans, who are also eight times more likely to develop blindness from glaucoma. Glaucoma appears to increase with age in the United States and decreases with age in Japan. Diabetic patients also have an increased risk for developing glaucoma.

The most common form of glaucoma in the United States is primary open-angle glaucoma, which accounts for about two thirds of all cases. In Asia the most common form of glaucoma is angle-closure glaucoma. Open-angle glaucoma tends to be genetically based, with multifactorial inheritance or as an autosomal recessive trait, with a high prevalence of carriers. Glaucoma is bilateral and occurs predominantly after age 50, although incidence is significant during the 30s and 40s, and it may even occur during the teenage years. Glaucoma is more severe in the African American population. Current incidence of glaucoma is 2% in the United States. The family physician can measure intraocular pressure using tonometry to detect elevated IOP. Tonometry can be performed with a Schi0tz tonometer, Perkins applanation tonometer, Tono-Pen XL tonometer, or Goldmann applanation tonometer held horizontally. This test should be performed at least every 3 years, beginning at age 35 years.

The damage to vision caused by glaucoma is irreversible. If the glaucoma can be detected early, it can usually be controlled and is curable by medial treatment, laser surgery, trabeculectomy, or some other filtering procedure. It is important to emphasize that glaucoma may occur at any age. Causes include congenital glaucoma, chronic open-angle glaucoma, narrow-angle glaucoma, or other forms of glaucoma, including pigmentary glaucoma.

One of the most common forms of secondary glaucoma is steroid glaucoma, which occurs in a substantial number of patients who use corticosteroid eyedrops or ointment for several weeks or longer. This condition also may occur with oral or systemic corticosteroid use, although it is rare. Steroid glaucoma is a form of open-angle glaucoma and, like primary open-angle glaucoma, can be effectively treated if detected early. If IOP is not lowered in time, there may be permanent damage to the optic nerve. Treatment for this type of glaucoma is discontinuation of corticosteroids and initiation of topical glaucoma medications. The IOP elevation is reversible once the steroids have been discontinued, but it may take 2 to 3 months or longer for pressure to return to a normal level. Any visual loss that occurs during this period may be permanent. There is no reliably safe dose of topical steroids that can ensure the prevention of steroid glaucoma. Even topical medications that consist of a combination of steroids and antibiotics or other type of medication can increase IOP. Because of the relative frequency of steroid glaucoma, as well as other ocular complications resulting from steroid use (e.g., cataract, exacerbation of viral infections), topical steroids should not be used for minor ocular inflammations, except in special circumstances.

Secondary glaucoma also may be caused by ocular trauma, intraocular inflammations, intraocular tumors, and carotid vascular disease. Regardless of cause, any patient suspected of having secondary glaucoma should be referred to an ophthalmologist as soon as possible for further evaluation and therapy. Management depends on the cause of the disease and character of the IOP elevation. Some medications can also result in glaucoma and include a warning related to developing angle-closure glaucoma. Additionally, topi-ramate (Topamax) is associated with an idiosyncratic acute glaucoma caused by uveal effusions.

With increased IOP, damage to the optic nerve and visual field abnormalities can occur. Almost all elevated pressures are caused by an obstruction to the outflow of aqueous humor. Aqueous humor, formed inside the eye in the ciliary body, circulates around the lens and through the pupil into the anterior portion of the eye. The aqueous humor exits through the anterior angle structures (trabecular meshwork and Schlemm's canal) (Fig. 41-35). About 10% of glaucoma cases occur in the setting of normal IOP, suggesting that these eyes are particularly susceptible to pressure changes. Glaucoma management involves more than controlling IOP. Possible sources of damage to the optic nerve involve mechanical factors affecting the optic nerve, decreased optic nerve perfusion, and blockage of axoplasmic flow in the lamina cribrosa. Carotid artery stenosis can also cause problems because of decreased perfusion to the optic nerve. Occasionally, elevations result from impeded outflow caused by elevated venous pressure, such as in patients with Sturge-Weber syndrome.

The most serious consequence of elevated IOP is damage to the optic nerve (Fig. 41-36). As IOP rises, retinal nerve

Anterior chamber

Angle of anterior chamber

Trabecula

Canal of Schlemm Aqueous vein

Anterior chamber

Trabecula

Canal of Schlemm Aqueous vein

Aqueous flow

Aqueous flow

Trabecula

Canal of Schlemm

Aqueous vein

Trabecula

Canal of Schlemm

Aqueous vein

Aqueous flow

B Ciliary body Angle open

Figure 41-35 A, Flow of aqueous from the ciliary body, leaving the eye through the trabecula and canal of Schlemm via a normal, open, wide angle. B, Chronic open-angle glaucoma. (From Scheie HG, Albert DM. Textbook of Ophthalmology, 9th ed. Philadelphia, Saunders, 1977.)

Aqueous flow

B Ciliary body Angle open

Figure 41-35 A, Flow of aqueous from the ciliary body, leaving the eye through the trabecula and canal of Schlemm via a normal, open, wide angle. B, Chronic open-angle glaucoma. (From Scheie HG, Albert DM. Textbook of Ophthalmology, 9th ed. Philadelphia, Saunders, 1977.)

fibers are destroyed at the optic nerve head, resulting in permanent visual loss. Peripheral vision is usually affected first, followed by progressive visual loss involving the entire visual field (Fig. 41-37).

KEY TREATMENT

Long-term monitoring is essential for successful management of glaucoma (AAO, 2000) (SOR: A).

For chronic open-angle glaucoma, initial treatment is topical medications (AAO, 2000) (SOR: C).

For uncontrolled chronic open-angle glaucoma, surgical treatment should be considered (AAO, 2000) (SOR: C).

For acute angle- closure glaucoma, medical treatment and surgery (laser or incision) should be implemented as soon as medically possible (Saw et al., 1993) (SOR: A).

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