Diagnosing and Treating Acute Anterior Uveitis, Part 1
BY WILLIAM L. MILLER, OD, PHD, FAAO
Uveitis affects between eight and 17 cases for each 100,000 people in the United States. About 25 years ago, the International Uveitis Study Group classified uveitis into one of three categories based on its anatomical location. Of these categories, anterior uveitis (iritis and iridocyclitis) represents the most frequent site of ocular inflammation, overshadowing its posterior counterpart by nearly four times. We can further subdivide the anatomical categories based on the temporal aspects of the inflammation (acute vs. chronic) and granulomatous or nongranulomatous, which may lend help when differentiating possible causes.
Uveitis symptoms include varying degrees of pain and photophobia. Patients frequently describe the pain as occurring in, around or even behind the eye. At times, they may describe it as a dull ache. Uveitis may affect vision, but it depends on the severity of the response and the magnitude of inflammatory cells.
Biomicroscopy reveals cells (leukocytes) and flare (protein leakage) in the anterior chamber. To elicit these signs, instruct the patient to move his eye up and down and to patiently wait in a darkened room for the cells to appear. You can further categorize uveitis into nongranulomatous and granulomatous based on the cellular components present, the former demonstrating lymphocytes and plasma cells and the latter epithelioid and giant cells. Nongranulomatous iritis can manifest keratic precipitates that are typically smaller (<0.5mm) than granulomatous counterparts.
Focus on Acute Anterior Uveitis
Initial cases of unilateral, solitary acute anterior uveitis (AAU) typically don't warrant continued investigation and may in fact be idiopathic. In cases of isolated anterior uveitis, it's important to make the patient comfortable by quelling the inflammatory reaction while simultaneously monitoring intraocular pressure.
The first line of treatment involves topical steroid drops tailored to the severity of the inflammatory reaction. Manage mild cases of anterior uveitis with 1% prednisolone acetate tid or qid, oftentimes combined with a cycloplegic agent (either 1% to 2% cyclopentolate or 5% homatropine). Handle moderate to severe cases with 1% prednisolone acetate every few hours, augmented with a cycloplegic agent 5% homatropine (bid, qid) or 0.25% scopolamine (bid).
Follow up in one day to one week, based on the level of inflammation. Carefully assess inflammation and monitor intra-
ocular pressure. Taper and then discontinue cycloplegic medication when the flare and cellular response start to subside. Continue topical steroids until both inflammatory signs are absent, at which point you can carefully taper the drops. During the tapering process, watch for rebounding effects of inflammation.
In the Genes
As mentioned, most cases of solitary AAU are idiopathic or related to traumatic events. However, a small subset will recur and result from a systemic disease. Continued work in this arena has shown a strong genetic connection, especially on chromosomes 6 and 9. A recent study (Martin et al, 2005) has shown a genetic region (9p21-9p24) that's closely associated with AAU in a group of ankylosing spondylitis patients. Genetics will undoubtedly aid future care, but in the meantime, it's our job to decrease inflammation and to give the ocular tissue a sporting chance.
For references, please visit
www.clspectrum.com/references.asp and click on document #114.
Dr. Miller is on the faculty at the University of Houston College of Optometry. He is a member of the American Optometric Association and serves on its Journal Review Board. You can reach him at
Contact Lens Spectrum, Issue: April 2005