Uveitis is defined as inflammation of the uveal tract—the iris, ciliary body, and choroid. However, the retina and fluid within the anterior chamber and vitreous are often involved as well. Most cases are idiopathic and presumed autoimmune; identifiable causes include trauma, infection, and systemic diseases, many of which are autoimmune. Symptoms include decreased vision, ocular ache, redness, photophobia, and floaters. Although uveitis is identified clinically, identifying the cause typically requires testing. Treatment depends on cause but typically includes topical, locally injected, or systemic corticosteroids with a topical cycloplegic-mydriatic drug. Noncorticosteroid immunosuppressive drugs may be used in severe and refractory cases.
Uveitis is classified anatomically as
Uveitis may occur with or without vitreitis, retinitis, papillitis, or optic neuritis.
Causes of anterior uveitis are
Causes of intermediate uveitis are
The latter five in this list are uncommon causes of intermediate uveitis.
Causes of posterior uveitis (retinitis) are
Causes of panuveitis are
Infrequently, systemic drugs cause uveitis (usually anterior). Examples are sulfonamides, pamidronate (an inhibitor of bone resorption), rifabutin, and cidofovir.
Systemic diseases causing uveitis and their treatment are discussed elsewhere in TheMANUAL.
Symptoms and Signs
Symptoms and signs may be subtle and vary depending on the site and severity of inflammation.
Anterior uveitis tends to be the most symptomatic, usually manifesting with
Signs include hyperemia of the conjunctiva adjacent to the cornea (ciliary flush or limbal injection). Slit-lamp findings include keratic precipitates (WBC clumps on the inner corneal surface), cells and flare (a haze) in the anterior chamber (aqueous humor), and posterior synechiae. With severe anterior uveitis, WBCs may layer in the anterior chamber (hypopyon).
Intermediate uveitis is typically painless and manifests with
The primary sign is cells in the vitreous humor. Aggregates and condensations of inflammatory cells often occur over the pars plana (near the junction of the iris and sclera), forming "snowballs." Vision may be decreased because of floaters or cystoid macular edema, which results from fluid leakage from blood vessels in the macula. Confluent and condensed vitreous cells and snowballs over the pars plana may cause a classic "snowbank" appearance, which can be associated with neovascularization of the retinal periphery.
Posterior uveitis may give rise to diverse symptoms but most commonly causes floaters and decreased vision as occurs in intermediate uveitis. Signs include
Panuveitis may cause any combination of the previously mentioned symptoms and signs.
Serious complications of uveitis include profound and irreversible vision loss, especially when uveitis is unrecognized, inadequately treated, or both.
The most frequent complications include
Uveitis should be suspected in any patient who has ocular ache, redness, photophobia, floaters, or decreased vision. Patients with anterior uveitis have ocular ache in the affected eye if light is shined in the unaffected eye (true photophobia), which is uncommon in conjunctivitis.
Diagnosis of anterior uveitis is by recognizing cells and flare in the anterior chamber. Cells and flare are seen with a slit lamp and are most evident when using a narrow, intensely bright light focused on the anterior chamber in a dark room. Findings of intermediate and posterior uveitis are most easily seen after dilating the pupil (see Ophthalmoscopy). Indirect ophthalmoscopy (usually done by an ophthalmologist) is more sensitive than direct ophthalmoscopy. (Note: If uveitis is suspected, patients should be referred immediately for complete ophthalmologic evaluation.)
Many conditions that cause intraocular inflammation can mimic uveitis and should be considered in the appropriate clinical settings. Such conditions include, most commonly, severe conjunctivitis (eg, epidemic keratoconjunctivitis), severe keratitis (eg, herpetic keratoconjunctivitis, peripheral ulcerative keratitis), and severe scleritis, and, less commonly, intraocular cancers in the very young (typically retinoblastoma and leukemia) and in the elderly (intraocular lymphoma). Much less commonly, retinitis pigmentosa (see Retinitis Pigmentosa) can manifest with mild inflammation, which may be confused with uveitis.
Treatment of active inflammation usually involves corticosteroids given topically (eg, prednisolone acetate 1% 1 drop q 1 h while awake) or by periocular or intraocular injection along with a cycloplegic-mydriatic drug (eg, homatropine 2% or 5% drops [if available] or cyclopentolate 0.5% or 1.0% drops, either drug given bid to qid depending on severity). Antimicrobial drugs are used to treat infectious uveitis. Particularly severe or chronic cases may require systemic corticosteroids (eg, prednisone 1 to 2 mg/kg po once/day), systemic noncorticosteroid immunosuppressive drugs (eg, methotrexate 15 to 20 mg po once/wk), laser phototherapy, cryotherapy applied transsclerally to the retinal periphery, or surgical removal of the vitreous (vitrectomy).
Last full review/revision October 2014 by Emmett T. Cunningham, Jr., MD, PhD, MPH
Content last modified October 2014