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Overview of Uveitis

By Kara C. LaMattina, MD, Assistant Professor of Ophthalmology, Boston University School of Medicine

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Uveitis is defined as inflammation of the uveal tract—the iris, ciliary body, and choroid. However, the retinal and fluid within the anterior chamber and vitreous are often involved as well. About half of cases are idiopathic; 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

  • Anterior uveitis: Localized primarily to the anterior segment of the eye, includes iritis (inflammation in the anterior chamber alone) and iridocyclitis (inflammation in the anterior chamber and anterior vitreous)

  • Intermediate uveitis: Localized to the vitreous cavity and/or pars plana

  • Posterior uveitis: Any form of retinitis, choroiditis, or inflammation of the optic disk

  • Panuveitis: Inflammation involving anterior, intermediate, and posterior structures

Uveitis is also classified by onset (sudden or insidious), duration (limited or persistent), and course (acute, recurrent, or chronic) (1)

General reference

Etiology

Causes of anterior uveitis include

Causes of intermediate uveitis include

Causes of posterior uveitis (retinitis) include

  • Idiopathic (most common)

  • CMV (in patients with HIV/AIDS)

  • HSV/VZV

  • Sarcoidosis

Causes of panuveitis include

  • Idiopathic (most common)

  • Sarcoidosis

  • TB

Infrequently, systemic drugs cause uveitis (usually anterior). Examples are sulfonamides, bisphosphonates (inhibitors of bone resorption), rifabutin, and cidofovir.

Systemic diseases causing uveitis and their treatment are discussed elsewhere in The MANUAL.

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 (especially when acute), usually manifesting with

  • Pain (ocular ache)

  • Redness

  • Photophobia

  • Decreased vision (to a variable degree)

Chronic anterior uveitis may have less dramatic symptoms and present with irritation or decreased vision.

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

  • Floaters

  • Decreased vision

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

  • Cells in the vitreous humor

  • White or yellow-white lesions in the retina (retinitis), underlying choroid (choroiditis), or both

  • Retinal vasculitis

  • Optic disk edema

Panuveitis may cause any combination of the previously mentioned symptoms and signs.

Complications

Serious complications of uveitis include profound and irreversible vision loss, especially when uveitis is unrecognized, inadequately treated, or both.

The most frequent complications include

  • Cataract

  • Glaucoma

  • Retinal detachment

  • Neovascularization of the retina, optic nerve, or iris

  • Cystoid macular edema (the most common cause of decreased vision in patients with uveitis)

  • Hypotony (an intraocular pressure that is too low to support the health of the eye)

Diagnosis

  • Slit-lamp examination

  • Ophthalmoscopy after pupil dilation

Uveitis should be suspected in any patient who has ocular ache, redness, photophobia, floaters, or decreased vision. Patients with unilateral 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 Evaluation of the Ophthalmologic Patient : 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 severe conjunctivitis (eg, epidemic keratoconjunctivitis), severe keratitis (eg, herpetic keratoconjunctivitis, peripheral ulcerative keratitis), and severe scleritis.

Acute angle closure glaucoma can cause redness and severe pain similar to that of uveitis, which is why it is important to check intraocular pressure at every visit. Uveitis is often (but not always) associated with a low intraocular pressure whereas pressure is typically high in acute angle closure glaucoma. Uveitis also can be distinguished from angle closure glaucoma by the absence of corneal haze and the presence of a deeper anterior chamber.

Other masqueraders include intraocular cancers in the very young (typically retinoblastoma and leukemia) and in the elderly (intraocular lymphoma). Much less commonly, retinitis pigmentosa can manifest with mild inflammation, which may be confused with uveitis.

Treatment

  • Corticosteroids (usually topical) and sometimes other immunosuppressive drugs

  • Cycloplegic-mydriatic drugs

  • Sometimes antimicrobial drugs

  • Sometimes surgical therapy

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 mg/kg po once/day), systemic noncorticosteroid immunosuppressive drugs (eg, methotrexate 15 to 25 mg po once/wk or adalimumab 40 mg every other week), laser phototherapy, cryotherapy applied transsclerally to the retinal periphery, or surgical removal of the vitreous (vitrectomy) (1).

Treatment reference

Key Points

  • Inflammation of the uveal tract (uveitis) can affect the anterior segment (including the iris), intermediate uveal tract (including the vitreous), or posterior uvea (including the choroid, retina, and optic nerve).

  • Most cases are idiopathic, but known causes include infections, trauma, and autoimmune disorders.

  • Findings in acute anterior uveitis include aching eye pain, photophobia, redness closely surrounding the cornea (ciliary flush), and, on slit-lamp examination, cells and flare.

  • Chronic anterior uveitis may have less dramatic symptoms and present with eye irritation or decreased vision.

  • Intermediate and posterior uveitis tend to cause less pain and eye redness but more floaters and decreased vision.

  • Diagnosis is confirmed by slit-lamp examination and ophthalmoscopic examination (often indirect) after pupillary dilation.

  • Treatment should be managed by an ophthalmologist and often includes corticosteroids and a cycloplegic-mydriatic drug along with treatment of any specific cause.

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