Primary Open Angle Glaucoma:
The vast majority of glaucoma patients have primary open angle glaucoma. These patients manifest a chronic, idiopathic disease associated with progressive degeneration of the anterior optic nerve, known as glaucomatous optic neuropathy. Although elevated intraocular pressure is an important causative risk factor, only half of the 2 to 3 million North Americans with glaucoma will manifest elevated intraocular pressure at a single measurement. Therefore, measurement of intraocular pressure alone is a poor screening technique for glaucoma. Like most biologic parameters, eye pressure fluctuates throughout the day and varies with other influences, including hydration, sleep, blood pressure and body position. With multiple measurements at different testing sessions, most, but not all of these glaucoma subjects, will eventually exhibit elevated intraocular pressure at least part of the time.
The rise in intraocular pressure associated with primary open angle glaucoma derives not from a visible obstruction of the trabecular meshwork, but rather from cellular dysfunction of the trabecular meshwork tissue, which leads to increased aqueous humor outflow resistance. Risk factors for primary open angle glaucoma include family history, corticosteroid sensitivity, myopia, African-American race, systemic high blood pressure, high intraocular pressure, diabetes, and age. In addition to these risk factors, early age of onset of disease and poor compliance with a medical regimen and physician visits are associated with a worse prognosis. As mentioned above, some patients with progressive optic nerve damage characteristic of glaucoma never manifest intraocular pressures above the statistically normal range. These patients are commonly diagnosed with "low pressure glaucoma,” “low tension glaucoma,” “or normal pressure glaucoma.” While recognizing that non-pressure risk factors may play a stronger role in these than in than in their high-pressure counterparts, these patients are managed similarly to those with conventional primary open angle glaucoma.
Closed Angle Glaucoma:
All physicians need be cognizant of another form of glaucoma, closed angle or angle-closure glaucoma, which may present acutely or may be silent and chronic. This disorder, quite unrelated to open angle glaucoma, derives entirely from blockade of the trabecular meshwork by the peripheral iris, either by simple and reversible anatomical apposition, or pressing together, of the two tissues or by generally irreversible scarring and adhesion. These irreversible fibrotic adhesions may occur after unrecognized long-standing appositional angle closure (chronic angle closure glaucoma) or from other ocular conditions, such as uveitis or neovascularization (secondary angle closure glaucomas).
Classically, angle closure glaucoma is the well known, less common variety of glaucoma that presents acutely with severe eye pain, blurring of vision, colored halos around lights, nausea and vomiting. Angle closure usually occurs in the hyperopic (farsighted) eye, which is smaller than the average eye and thus crowds the iris, cornea, lens and anterior chamber angle into a smaller than average space. Eventually, usually in the fifth to sixth decade of life as the lens gradually increases in size with aging, the lens becomes more firmly applied to the pupillary opening through which aqueous humor from the ciliary body must pass. This obstruction of aqueous humor flow at the pupil, known as relative pupillary block, eventually becomes clinically significant and traps the aqueous behind the pupil, raising the pressure in the posterior chamber above that in the anterior chamber and driving the iris anteriorly to lie against and block the trabecular meshwork. This trabecular meshwork blockade, or angle closure, leads to a sudden and dramatic rise of the intraocular pressure from its baseline normal level in the 10-20 mm Hg range to 60 mm Hg or more. This sudden change in pressure leads to swelling of the cornea with blurring, haloes, and severe ocular pain from iris ischemia and corneal edema. The pupillary margin of the iris becomes most tightly applied to the lens surface when the pupil is in the mid-dilated position; hence, it is often dilation of the pupil by exposure to stress, darkness, or drugs that precipitates an acute attack.
The immediate treatment of acute angle closure is directed toward reversal of the pupillary block, usually by moving the pupil with constriction. Ultimately, however, the pupillary block can be reversed and prevented by creating a new aqueous channel with peripheral iridectomy. (see Treatment)