Definition
Inflammation of the anterior uveal tract (iris and ciliary body), the most common form of uveitis, characterized by anterior chamber cells and flare, keratic precipitates, and variable degrees of photophobia and pain.
Clinical Snapshot
Anterior uveitis (AU) — also termed iritis or iridocyclitis — is the most common form of uveitis, accounting for approximately 75% of all uveitis cases. It is defined by inflammation of the iris and/or ciliary body, with cells and flare in the anterior chamber as the hallmark finding. The majority of cases are idiopathic or HLA-B27–associated. Recurrent AU in a young adult should prompt systemic evaluation for HLA-B27–associated spondyloarthropathies. Prompt treatment with topical corticosteroids and cycloplegics prevents complications including posterior synechiae, cataract, and secondary glaucoma.
Epidemiology
AU has an annual incidence of approximately 8–12 per 100,000 and a prevalence of approximately 69 per 100,000. It is the most common form of uveitis in developed countries. HLA-B27 is present in approximately 50% of patients with recurrent AU, compared to approximately 8% of the general population.
Pathophysiology
AU results from breakdown of the blood-aqueous barrier, allowing inflammatory cells and protein (flare) to enter the anterior chamber. In HLA-B27–associated AU, molecular mimicry between bacterial antigens (particularly Klebsiella pneumoniae) and HLA-B27 is hypothesized to trigger the autoimmune response. Granulomatous AU (large "mutton-fat" KPs) is associated with sarcoidosis, VKH, and sympathetic ophthalmia. Non-granulomatous AU (fine KPs) is associated with HLA-B27 spondyloarthropathies and herpetic disease.
Risk Factors
Clinical Presentation
Acute onset of unilateral photophobia, pain, and blurred vision. Circumlimbal (ciliary) injection. Slit lamp: anterior chamber cells (graded 0–4+) and flare (protein), keratic precipitates (KPs) on the corneal endothelium, posterior synechiae (iris adhesions to the anterior lens capsule). Hypopyon in severe cases. IOP may be elevated (trabeculitis) or reduced (ciliary body shutdown).
Diagnostic Pearls
Differential Diagnosis
Evidence-Based Management
Topical corticosteroids: prednisolone acetate 1% (Pred Forte®) — frequency titrated to cell grade (hourly for severe, QID for mild). Cycloplegics: cyclopentolate 1% or homatropine 5% — reduce pain, prevent posterior synechiae, and stabilize the blood-aqueous barrier. Taper corticosteroids slowly based on cell resolution — premature taper is the most common cause of recurrence. Periocular or systemic corticosteroids for severe or refractory cases. Systemic immunosuppression (methotrexate, mycophenolate) for chronic or recurrent disease.
Monitoring & Follow-Up
Follow up every 1–2 weeks during active inflammation. Monitor IOP at every visit — both corticosteroid-induced elevation and hypotony from ciliary body shutdown are possible. Dilated examination to assess for posterior synechiae, cataract, and CME.
Clinical Pearls
Related Therapeutics — Clinician's Companion
Key References
This entry is an educational reference designed to support clinical reasoning and awareness. It does not constitute medical advice, establish a standard of care, or replace individualized patient assessment. Clinicians should consult current guidelines and applicable clinical resources when making patient care decisions.