In 1813, Joseph Beer first reported the association of uveitis and glaucoma, describing it as arthritic iritis followed by glaucoma and blindness. In 1891, Priesley Smith proposed the first modern classification of uveitic glaucoma. Later, specific types of uveitic glaucoma were described by Fuchs in 1906 (Fuchs heterochromic uveitis) and Posner and Schlossman in 1948 (glaucomatocyclitic crisis).
The mechanisms by which uveitis leads to elevated intraocular pressure (IOP) are numerous and poorly understood. In general, iridocyclitis affects both aqueous production and resistance to aqueous outflow, with the subsequent change in IOP representing a balance between these two factors. Inflammation of the ciliary body usually leads to reduced aqueous production, and combined with increased uveoscleral outflow often seen in inflammatory states, hypotony often is a consequence.
Prostaglandins, which have been demonstrated to be present in the aqueous of eyes with uveitis, are known to cause elevated IOP without a reduction in outflow facility. Mechanisms of increased resistance to aqueous outflow with both acute and subacute forms of uveitis usually are of the open-angle type and include obstruction of the trabecular meshwork by inflammatory cells or fibrin, swelling or dysfunction of the trabecular lamellae or endothelium, and inflammatory precipitates on the meshwork. Uveitis also may be associated with secondary angle-closure glaucoma.
Alteration of the protein content of the aqueous humor may be a cause of elevated IOP in uveitis. Increased levels of protein in the aqueous are a result of increased permeability of the blood-aqueous barrier, which leads to an aqueous that more closely resembles undiluted serum. This elevated protein content may, in fact, lead to aqueous hypersecretion and IOP elevation.
The treatment of the uveitis can lead to elevated IOP. Although corticosteroids have proven to be effective in relieving inflammation, prolonged administration can result in elevated IOP. Corticosteroids increase IOP by decreasing aqueous outflow. Several theories have been proposed to explain this phenomenon, including accumulation of glycosaminoglycans in the trabecular meshwork, inhibition of phagocytosis by trabecular endothelial cells, and inhibition of synthesis of certain prostaglandins.
The prevalence of uveitis has been estimated at approximately 115 people per 100,000 in the United States. Approximately 20% of uveitis patients develop glaucoma.
The prevalence of uveitis has been estimated at 38-730 people per 100,000 worldwide. Approximately 20% of uveitis patients develop glaucoma.
Acute iridocyclitis usually produces symptoms; however, subacute iridocyclitis produces few or no symptoms but can have serious consequences because its complications may go undetected until advanced damage has occurred. If the inflammation is not controlled promptly, posterior synechiae and peripheral anterior synechiae (PAS) can form, leading to progressive angle closure and irreversible optic nerve damage.
No known racial predilection exists.
No known sexual predilection exists.
No known age predilection exists.
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- Medication Summary
- Carbonic anhydrase inhibitors
- Adrenergic agonists
- Prostaglandin analogs
- Nonsteroidal anti-inflammatory agents
- Topical corticosteroids
- Nonsteroidal Anti-Inflammatory Drug (NSAID), Ophthalmic
- Corticosteroid, Ophthalmic
- Beta-blocker / Alpha Agonist Combination
- Carbonic Anhydrase Inhibitor
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