eMedicine Specialties > Ophthalmology > Intraocular Pressure

Glaucoma, Uveitic

Author: Leon Herndon Jr, MD, Associate Professor, Department of Ophthalmology, Duke University Medical Center
Contributor Information and Disclosures

Updated: Apr 14, 2006

Introduction

Background

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).

Pathophysiology

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 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.

Frequency

United States

Rare

International

Rare

Mortality/Morbidity

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.

Race

No known racial predilection exists.

Sex

No known sexual predilection exists.

Age

No known age predilection exists.

Clinical

History

Symptoms with acute iridocyclitis may include blurred vision, ocular pain, brow ache, and other ocular disturbances.

• Blurred vision: It often is difficult to know if the blurred vision is due to glaucoma, uveitis, or complications associated with the uveitis.
• Ocular pain: Pain is a frequent finding in acute iridocyclitis but often is not seen with subacute or chronic iridocyclitis. Some patients with markedly elevated IOP often have severe eye pain associated with corneal edema.
• Brow ache: Ocular pain associated with elevated IOP often is referred to the brow on the affected side.
• Ocular disturbances: Other ocular disturbances (eg, photophobia, colored halos) may be associated with acute iridocyclitis and corneal edema, respectively.

Physical

• The cornea may reveal band keratopathy, epithelial dendrites, or stromal scarring from herpetic infections. Corneal epithelial edema associated with acutely elevated IOP may give rise to a steamy appearance. Keratic precipitates may be present on the endothelium and have different characteristics that signify various diagnoses.
• The hallmark of anterior uveitis is the presence of cells and flare in the anterior chamber. Cellular infiltration is due to release of chemotactic factors into the anterior chamber, and flare results from leakage of protein into the anterior chamber.
• The iris should be examined for evidence of stromal atrophy, nodules, and posterior synechiae and PAS. Inflammation can result in engorgement of the blood vessels in both the iris stroma and the angle, which can be confused with rubeosis iridis.
• The lens may have pigment on the anterior capsule, and posterior subcapsular opacification may be due to uveitis or to chronic corticosteroid therapy.
• The vitreous cavity may show the presence of cells or snowball opacities.
• The IOP may be low, normal, or high due to variations in aqueous secretion, amount of outflow obstruction, and dose of corticosteroids being used.
• Gonioscopy should be performed to detect the presence of PAS and to assess the degree of angle closure.
• The posterior segment should be examined, paying particular attention to the optic nerve to document morphologic changes consistent with glaucoma. Other possible posterior segment findings include cystoid macular edema, retinitis, perivascular sheathing, choroidal infiltrates, or retinal detachment.

Causes

Many specific uveitic entities may lead to the development of glaucoma. Some of the more common syndromes are listed below.

• Juvenile rheumatoid arthritis
  • Juvenile rheumatoid arthritis (JRA) is defined as an arthritis, with a duration of at least 3 months, that begins prior to age 16 years and is diagnosed after exclusion of other causes of arthritis.
  • Glaucoma is a common complication of chronic uveitis in patients with JRA and most frequently is caused by progressive closure of the angle by PAS.
  • Since the uveitis frequently is treated with prolonged topical corticosteroids, steroid-induced glaucoma may occur. The reported incidence of glaucoma varies from 14-22%.
• Fuchs heterochromic iridocyclitis
  • Fuchs heterochromic iridocyclitis (FHI) usually is unilateral and appears between the third and fourth decades with the insidious onset of mild, chronic anterior uveitis that usually is asymptomatic.
  • The glaucoma associated with FHI resembles primary open-angle glaucoma.
  • Gonioscopic evaluation may reveal multiple fine blood vessels, arranged either radially or concentrically in the trabecular meshwork.
  • Cataract is a constant feature of FHI, whereas glaucoma has been reported to occur in 6-47% of cases.
  • The uveitis does not need treatment with anti-inflammatory or immunosuppressive agents.
• Posner-Schlossman syndrome is characterized by a number of unusual features, including unilateral involvement, recurrent attacks of often very mild cyclitis, marked elevation of IOP, open angle, and occasional heterochromia. The condition typically affects individuals aged 20-50 years and resolves spontaneously regardless of treatment.
• Herpetic uveitis
  • Herpes simplex
    • Ocular manifestations of herpes simplex virus have been classified in accordance with the site of the corneal involvement and the presence or absence of associated uveitis, including herpetic superficial keratitis, disciform keratitis, disciform keratouveitis, and necrotic stromal keratitis. Disciform keratouveitis and necrotic stromal keratitis are associated more commonly with elevated IOP than epithelial keratitis.
    • The elevated IOP may be caused by trabeculitis, inflammatory obstruction of the trabecular meshwork, and angle closure in severe keratouveitis. The management of elevated IOP initially is directed toward controlling the viral replication and inflammation.
  • Varicella zoster
    • Ocular involvement of cutaneous varicella zoster occurs in two thirds of patients when the ophthalmic division of the trigeminal nerve is involved. Dendritic keratitis, stromal keratitis, and exposure keratitis are common.
    • IOP elevation and glaucoma are believed to be caused by decreased outflow facility due to trabecular obstruction from inflammatory debris, trabeculitis, and damage to the trabecular meshwork by recurrent inflammation. Treatment with systemic acyclovir when the cutaneous lesions are still active appears to reduce the risk of elevated IOP.

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