Diagnostic Summary

General Considerations

Glaucoma refers to increased intraocular pressure (IOP) as a result of an imbalance between production and outflow of the aqueous humor. Obstruction to outflow is the main factor responsible for this imbalance in closed-angle glaucoma. Acute glaucoma can occur only with the closure of a preexisting narrow anterior chamber angle, while in chronic open-angle glaucoma the anterior chamber appears normal.

In the United States, approximately 3 million people have glaucoma, which is undetected in 25% of them.¹ The chronic open-angle type, for which there appears to be no consistent anatomic basis, accounts for 70% to 75% of these cases. Histologically, however, there is a strong correlation between the content and composition of collagen and the glaucomatous eye.²

Collagen is the most abundant protein in the body, including the eye. In the eye it provides tensile strength and integrity to the tissues (e.g., cornea, sclera, lamina cribrosa, trabecular meshwork, vitreous). Inborn errors of collagen metabolism (e.g., osteogenesis imperfecta, Ehlers-Danlos syndrome, Marfan syndrome) are often associated with ocular complications: glaucoma, myopia, retinal detachment, ectopia lentis, and blue sclera.³ Morphologic changes in the lamina cribrosa (the scleral area that is pierced by the optic nerve fibers and blood vessels), trabecular meshwork (the connective tissue network through which aqueous humor must pass to reach the canal of Schlemm), and papillary blood vessels in the eye have all been observed in glaucomatous eyes.^2,4–6 These changes may result in elevated IOP readings or, perhaps more significantly, lead to the progression of peripheral visual loss. Changes in collagen structure would explain the following^2,4–6:

In some cases glaucoma develops in people with normal IOP. Referred to as low-tension glaucoma or normotensive glaucoma, this form accounts for approximately 25% to 30% of all cases of glaucoma in the United States. Because elevated IOP is not a factor in normal-tension glaucoma, other factors must be responsible for the optic nerve damage. Suggested causes include:

Normotensive glaucoma is more common in women than in men and affects adults averaging 60 years of age. A common risk factor for normotensive glaucoma is low blood pressure.

Diagnosis

Patients with open-angle glaucoma initially have no symptoms, which is why this disease can be so insidious. Physical examination may reveal slight cupping of the optic disc and narrowing of the visual fields. Tonometry is key to confirmation of the diagnosis.

The primary challenge with acute glaucoma is early recognition, because delay in referral for surgical intervention increases the risk of blindness. Table 168-1 provides an overview of the differential diagnosis of the inflamed eye.

TABLE 168-1 Differential Diagnosis of the Inflamed Eye

Therapeutic Considerations

Treatment and prevention of both acute and chronic glaucoma depend on the reduction of IOP and improvement of collagen metabolism, particularly in the optic disc and trabecular meshwork.

The optic disc is composed of the lamina cribrosa, optic nerve fibers, and blood vessels. The lamina cribrosa is a meshlike network rich in collagen through which the optic nerves and blood vessels must pass. The morphologic changes in the collagen of the eye (i.e., lamina cribrosa, papillary vessels, and trabecular meshwork) precede pressure changes. Therefore, primary prevention of breakdown of the ground substance and collagen framework is important here, as it is in other conditions involving collagen abnormalities (i.e., atherosclerosis, rheumatoid arthritis, and periodontal disease).

Supplements and Diet

Vitamin C

Of foremost importance in achieving collagen integrity are optimal tissue concentrations of ascorbic acid (AA). Furthermore, AA has been demonstrated to lower IOP levels in many clinical studies.^7–11 A daily dose of 0.5 g/kg, whether in single or divided doses, reduces the IOP by an average of 16 mm Hg.¹¹ Near normal tension levels were achieved in some patients unresponsive to acetazolamide (a carbonic anhydrase inhibitor) and 2% pilocarpine (a miotic agent).¹¹

The hypotonic action of AA on the eye is long-lasting if supplementation is continued, and intravenous administration results in an even greater initial reduction in IOP.^7,9–11 The patient must be monitored to determine the appropriate individual dose, because some patients respond to as little as 2 g/day, whereas others will respond only to extremely high doses (e.g., 35 g/day).^7–11 Abdominal discomfort as a side effect of high doses is common but usually resolves after 3 to 4 days.¹¹

The proposed mechanisms by which AA lowers IOP include the following:

• Increased blood osmolarity

• Diminished production of aqueous fluid by the ciliary epithelium

• Improved outflow of aqueous fluid

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