Glaucoma

A group of ocular conditions characterized by optic nerve damage which is related to the IOP (normal range: 10-21 mmHg) caused by congestion of aqueous humor in the eye. It is more prevalent among people older than 49 years of age, and the incidence increases with age. Two major forms 1. Acute (angle-closure)  It may result from trauma, stress, or any process that pushes the iris forward against the inside of the cornea when there is already an anatomically shallow anterior chamber.  Acute glaucoma results when the angle between the iris and the cornea becomes narrowed restricting or blocking the drainage of aqueous humor through the trabecular network and canal of Schlemm causing the IOP to increase suddenly.  It is an acute, painful condition that can cause permanent eye damage within several hours. 2. Chronic (open-angle) glaucoma  It results from the gradual deterioration of the trabecular network that, as in the acute form, blocks drainage of aqueous humor and causes IOP to increase.  Untreated, this results in degeneration of the optic nerve and visual field loss. Chronic glaucoma is the most common form of glaucoma, and its incidence increases with age. Genetics and conditions, such as diabetes and hypertension, also play a role.

Predisposing Factors: o Family History o African-American Race o Older Age

Precipitating Factors: o Infection o Tumor o Hemorrhage o Prolonged use of topical or systemic corticosteroids o Cardiovascular Disease o Diabetes o Migraine Syndrome o Eye trauma o Hypertension

 Narrow angles between the anterior iris and posterior corneal surface  Shallow anterior chambers  Thickened iris

Obstruction in the trabecular meshwork - Chronic Glaucoma

Closure of the anterior chamber angle of the eye (complete or incomplete) - Acute Glaucoma

Obstruction in the flow of aqueous humor

Prevent outflow of aqueous humor

IOP

Optic nerve compression

Impaired Blood flow

Atrophy of the optic nerve (characterized by loss of nerve fibers & blood supply)

Progressive loss of vision

Visual field defects