Anterior Uveitis

Circumlimbal flush in anterior uveitis.

Signs and Symptoms: The typical presentation of anterior uveitis involves pain, photophobia and hyperlacrimation. Patients report a deep, dull aching of the involved eye and surrounding orbit. Associated sensitivity to lights may be severe. Excessive tearing results secondary to increased neural stimulation of the lacrimal gland, and is not associated with a foreign-body sensation.

Visual acuity is variable, ranging from mild blur to significant vision loss if synechia or a cyclitic membrane are present. External exam may reveal mild to moderate lid swelling, resulting in pseudoptosis. A deep, perilimbal injection of the conjunctiva and episclera is typical, while the palpebral conjunctiva is characteristically normal. The cornea may display mild edema upon biomicroscopy.

The hallmark signs of anterior uveitis are cells and flare in the anterior chamber. If the anterior chamber reaction is significant, small gray to brown endothelial deposits known as keratic precipitates may arise. This can then lead to endothelial cell dysfunction and the corneal edema.

Iris findings may include adhesions to the lens capsule (posterior synechia) or, less commonly, to the peripheral cornea (anterior synechia). Additionally, granulomatous nodules may appear on the surface of the iris stroma. Intraocular pressure is initially reduced in the involved eye, due to secretory hypotony of the ciliary body. However, as the reaction persists, inflammatory by-products may accumulate in the trabeculum. If this debris builds significantly, and if the ciliary body resumes its normal secretory output, the pressure may rise sharply, resulting in a secondary uveitic glaucoma.

Pathophysiology: Uveitis, as the name implies, represents an inflammation of the uveal tissues, chiefly the iris and ciliary body. This inflammation may be associated with underlying systemic disease or autoimmunity, or it may occur as a direct result of ocular trauma. Occasionally, inflammatory reactions in adjacent tissues--for example, keratitis--can induce a secondary uveitis.

Both acute and chronic forms of anterior uveitis are clinically recognizable. The chronic form is more often associated with a host of systemic disorders (see table). Chronic uveitis most likely occurs due to an immunopathological mechanism that is not fully understood.

Management: Your two primary goals in the manage ment of anterior uveitis should be to first immobilize the iris to decrease the pain and prevent synechia, and to aggressively quell the inflammatory response.

Keratic precipitates in anterior uveitis.

Cycloplegia is in order. Use either scopolamine 0.25% bid-qid, or atropine 1% bid, depending upon the severity of the reaction. Prescribe topical steroids, such as prednisolone acetate 1%, at least q1-2h initially, even more frequently if warranted. We commonly employ a loading dose of one drop every 15 minutes for six hours, then taper to q1-2h. If posterior synechia is present, attempt to break the adhesions in the office using 1% atropine in conjunction with 10% phenylephrine. Address significant secondary elevations in IOP (>26mm Hg) with standard aqueous suppressant agents. Avoid pilocarpine in uveitic glaucoma because it will only worsen the inflammatory response by mobilizing the uveal tissues. Likewise, avoid prostglandin-like medications. After you initiate treatment, re-evaluate patients every 1-7 days, depending on the severity of the reaction. As the condition resolves, you may discontinue the cycloplegics and taper the topical steroids to qid or tid. Generally, it is better to taper slowly rather than abruptly; patients may need to remain on steroid drops daily or every other day for several weeks to months. In recalcitrant cases of uveitis that do not respond to conventional therapy, injectable depot steroids (e.g., methylprednisolone 60mg), oral corticosteroids (prednisone 60-80mg), or other immunosupressant medications are indicated.

Clinical Pearls:

Systemic Disorders Associated With Chronic Uveitis • Ankylosing spondylitis. • Behçet's syndrome. • Inflammatory bowel disease. • Juvenile rheumatoid arthritis. • Reiter's syndrome. • Sarcoidosis. • Syphilis. • Tuberculosis. • Lyme disease.

• Acute anterior uveitis that we see in optometric practice results most commonly from blunt ocular trauma. In most instances, these cases resolve without incident and do not recur when properly managed.
• Consider recurrent uveitis--defined as three or more unexplained incidents--secondary to underlying systemic inflammatory disease until proven otherwise.
• Hematological testing is indicated for any recurrent, chronic, or bilateral presentation. A standard battery of laboratory tests should include: complete blood count (CBC) with differential; antinuclear antibody (ANA); HLA-B27; rheumatoid factor (RF); angiotensin-converting enzyme (ACE); purified protein derivative (PPD); fluorescent treponemal antibody absorption (FTA-ABS); and rapid plasma reagin (RPR). A chest X-ray is important for identifying sarcoidosis and tuberculosis.
• Treat aggressively and follow closely. The goal of therapy is to have no cells with the patient on little or no steroids, and to have no therapy-related complications.
• One additional point: Always perform a comprehensive, dilated fundus evaluation in these cases. Anterior uveitis may actually constitute a "spillover" of posterior ocular inflammation.

Other reports in this section

• Crystalline Lens Subluxation
• Ciliary-Block Glaucoma
• Primary Open-Angle Glaucoma
• Pigment Dispersion Syndrome and Pigmentary Glaucoma
• Pseudoexfoliation Syndrom and Pseudoexfoliative Glaucoma
• Anterior Uveitis