SIGNS AND SYMPTOMS
The typical presentation of anterior uveitis involves pain, photophobia and excessive tearing. Patients report a deep, dull aching of the involved eye and surrounding orbit. Associated sensitivity to lights may be severe; often, these patients will present wearing dark sunglasses. The excessive tearing occurs secondary to increased neural stimulation of the lacrimal gland, and is not associated with a foreign body sensation.

Visual acuity is not usually impaired to any great extent (20/40 or better is common), although patients may report some haziness. Accommodative tasks, however, may prove more difficult and uncomfortable. Inspection may reveal mild to moderate congestion of the lids, resulting in pseudoptosis. You'll typically see a deep perilimbal injection of the conjunctiva and episclera, although the palpebral conjunctiva is characteristically normal. The cornea may display mild edema upon biomicroscopy. In more severe reactions, you may observe grayish brown endothelial deposits, known as keratic precipitates.

The hallmark signs of anterior uveitis are "cells and flare." Cells are leukocytes (white blood cells) floating in the convection currents of the aqueous; flare refers to liberated protein from the inflamed iris or ciliary body which gives the aqueous a particulate, or smoky, appearance. The iris may adhere to the lens capsule (posterior synechia) or, less commonly, to the peripheral cornea (anterior synechia). Additionally, you may see granulomatous nodules within the iris stroma.

Intraocular pressure in the affected eye is initially reduced 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. Inflammation may be associated with underlying systemic disease, or it may occur as a direct result of ocular trauma. Occasionally, inflammatory reactions in adjacent tissues (e.g., keratitis), can induce a secondary uveitis.

Uveitis can be either acute or chronic. The chronic form is more often associated with systemic disorders including, but not limited to, ankylosing spondylitis, Behçet's syndrome, inflammatory bowel disease, juvenile rheumatoid arthritis, Reiter's syndrome, sarcoidosis, syphilis, tuberculosis, and Lyme disease. Chronic uveitis most likely occurs due to an immunopathological mechanism which is not fully understood.

MANAGEMENT
There are two primary goals when managing anterior uveitis. First, immobilize the iris and ciliary body to decrease pain and prevent exacerbation of the condition. Second, quell the inflammatory response. Begin by cyclopleging the patient with homatropine 5% TID/QID, scopolamine 0.25% BID/QID or atropine 1% BID, depending upon the severity of the reaction. Next, prescribe a topical steroid Q2-3H, or more often if the reaction is severe. If there's a posterior synechia present, attempt to break the adhesion in the office using atropine 1% and phenylephrine 10%. Treat secondary elevations in IOP using standard anti-glaucoma agents, such as timolol 0.5% BID or dorzolamide 2% TID.

Avoid pilocarpine in uveitic glaucoma, as it will only serve to worsen the inflammatory response by mobilizing the uveal tissues. After beginning treatment, re-evaluate the patient every one to seven days depending on the severity of the reaction. As the uveitis resolves, discontinue the cycloplegics and taper the steroids to QID or TID. Generally, it is better to taper slowly rather than abruptly, and patients may need to remain on steroid drops daily or every other day for several weeks. In recalcitrant uveitis which is unresponsive to conventional therapy, consider injectible steroids such as methylprednisolone 60mg or even oral steroids such as prednisone 60 to 80mg.

CLINICAL PEARLS

• Acute anterior uveitis results most commonly as a result of blunt ocular trauma. In most instances, these cases resolve without incident and do not recur when properly managed.

• Consider any cases of recurrent uveitis, defined as three or more unexplained incidents, to be representative of underlying systemic inflammatory disease until proven otherwise. Hematologic 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 also important in identifying both sarcoidosis and tuberculosis. A Lyme titer is also recommended if you suspect that the patient may have been bitten by a deer tick.

• 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

• Primary Open Angle Glaucoma
• Uveitic Glaucoma & Glaucomatocyclitic Crisis
• Pigment Dispersion Syndrome & Pigmentary Glaucoma
• Acute Angle Closure Glaucoma
• Anterior Uveitis
• Hyphema
• Angle Recession Glaucoma
• Lens Induced Glaucoma
• Pseudoexfoliation Syndrome and Pseudoexfoliative Glaucoma
• Axenfeld-Rieger Syndrome
• Neovascular Glaucoma
• Pars Planitis
• Choroidal Rupture