Загальні відомості про увеїт

Causes of anterior uveitis include

• Idiopathic or postsurgical (most common cause)

• Trauma

• Spondyloarthropathies

• Juvenile idiopathic arthritis

• Herpesvirus infection (herpes simplex virus [HSV], varicella-zoster virus [VZV], and cytomegalovirus [CMV])

• Tubulointerstitial nephritis and uveitis (TINU)

Causes of intermediate uveitis include

• Idiopathic (most common)

• Multiple sclerosis

• Sarcoidosis

• Tuberculosis (TB)

• Syphilis

• Lyme disease (in endemic regions)

Causes of posterior uveitis (retinitis) include

• Idiopathic (most common)

• Toxoplasmosis

• CMV (in immunocompromised patients)

• HSV/VZV

• Sarcoidosis

• Syphilis

• TB

Causes of panuveitis include

• Idiopathic (most common)

• Sarcoidosis

• TB

• Vogt-Koynagi-Harada syndrome (VKH)

• Syphilis

Infrequently, systemic medications cause uveitis (usually anterior). Examples are sulfonamides, bisphosphonates (inhibitors of bone resorption), rifabutin, cidofovir, antivascular endothelial growth factor (anti-VEGF) agents, and chemotherapy agents, including checkpoint inhibitors and BRAF/MEK protein kinase inhibitors.

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 such as irritation or decreased vision, or symptoms may be absent.

Signs include hyperemia of the conjunctiva adjacent to the cornea (ciliary flush or limbal injection). Slit-lamp findings include keratic precipitates (white blood cell clumps on the inner corneal surface), cells and flare (a haze) in the anterior chamber (aqueous humor), and posterior synechiae. With severe anterior uveitis, white blood cells may layer in the anterior chamber (hypopyon).

Uveitis (Anterior)

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Image courtesy of Sunir Garg, MD.

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, appearing as "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 (part of the ciliary body that extends posteriorly beyond the junction of the iris and sclera) may cause a classic "snowbank" appearance, which can be associated with neovascularization of the retinal periphery (1).

Uveitis (Intermediate)

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© Springer Science+Business Media

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 (with whitening or obliteration of blood vessels)

• Optic disk edema

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

• Slit-lamp examination

• Ophthalmoscopy after pupil dilation

Uveitis should be suspected in any patient who has ocular ache, redness, photophobia, new onset or changing 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. 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 older adults (intraocular lymphoma). Much less commonly, retinitis pigmentosa can manifest with mild inflammation, which may be confused with uveitis.

• Corticosteroids (usually topical) and sometimes other immunosuppressive medications

• Cycloplegic-mydriatic medications

• Sometimes antimicrobial medications

• Sometimes surgical therapy

Treatment of active inflammation usually involves corticosteroids given topically (eg, prednisolone acetate 1% one drop as frequently as every hour while awake for severe inflammation) or by periocular or intraocular injection along with a cycloplegic-mydriatic medication (eg, homatropine 2% or 5% drops or cyclopentolate 0.5% or 1.0% drops, either medication given 2 to 4 times/day depending on severity). Corticosteroid implants are available that can treat both active inflammation in the eye as well as uveitic macular edema. They are not associated with systemic symptoms, but they can accelerate cataract formation as well as cause ocular hypertension (1). Antimicrobial drugs are used to treat infectious uveitis.

Particularly severe or chronic cases may require systemic corticosteroids or systemic noncorticosteroid immunosuppressive medications. For example,

• Prednisone 1 mg/kg orally once/day

• Systemic noncorticosteroid immunosuppressive medications (eg, methotrexate 15 to 25 mg orally once/week; mycophenolate mofetil 500 mg twice daily for 2 weeks, followed by a maintenance dose of 1 to 1.5 g orally twice daily as tolerated; adalimumab, initial dose of 80 mg, followed by 40 mg subcutaneously every 1 to 2 weeks)

• Infliximab 5 to 10 mg/kg IV every 4 weeks

Additional treatment for severe or chronic cases may require laser phototherapy, cryotherapy applied transsclerally to the retinal periphery, or surgical removal of the vitreous (vitrectomy) (2–4).