Glaucoma is characterized by increased intraocular pressure that may cause impaired vision, ranging from slight loss to absolute blindness. Adequate lowering of intraocular pressure almost always stops optic nerve damage. In chronic open-angle glaucoma, aqueous secretion by the ciliary body is normal, and its flow between the lens and the iris through the pupil into the anterior chamber is normal; however, the trabecular meshwork does not permit adequately rapid egress of aqueous with a resultant pressure elevation.
The most common cause of glaucoma is impaired outflow through the trabecular meshwork. It can also be caused by obstruction to the outflow from Schlemm's canal and the aqueous veins created by elevated orbital venous pressure (as in AV malformations, orbital congestion due to thyroid disease, etc.). Excessive aqueous secretion is an extremely rare cause.
Secondary glaucoma is caused by any interference with the flow of aqueous humor from the posterior chamber through the pupil into the anterior chamber to the canal of Schlemm. Inflammatory disease of the anterior segment (uveitis) may prevent aqueous escape by causing complete posterior synechia and iris bombˇ and may plug the drainage channel with exudates. Other common causes are intraocular tumors, enlarged intumescent cataracts, central retinal vein occlusion, trauma to the eye, operative procedures, and intraocular hemorrhage. Prolonged corticosteroid therapy, especially with topical ophthalmic preparations, can produce an increased pressure, particularly in patients with a predisposition, so-called steroid responders.
Risk factors for glaucoma include: Positive family history, Diabetes mellitus, and African-American ancestry.
Glaucoma is diagnosed with an ophthalmoscope, which shows damage to the optic nerve head.
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