A red, painful, light-sensitive eye that keeps coming back is not just conjunctivitis. Uveitis is inflammation inside the eye itself, and it needs specialist care to protect vision long-term.

Uveitis is inflammation of the uveal tract, the middle layer of the eye that includes the iris, the ciliary body, and the choroid. When this tissue becomes inflamed, the consequences range from a painful red eye that resolves quickly with treatment, to a chronic smoldering process that silently damages the retina and optic nerve over years. Uveitis is one of the most common causes of preventable blindness in working-age adults in developed countries, and it is frequently misdiagnosed or undertreated because it can mimic simpler conditions and its behaviour is unpredictable. The key to preserving vision is accurate diagnosis, appropriate treatment, and long-term monitoring.

What You Need to Know About Uveitis

Uveitis is classified by anatomical location: anterior (front of the eye, most common), intermediate (mid-vitreous), posterior (retina and choroid), and panuveitis (all layers)
Posterior and panuveitis carry the greatest risk of permanent vision loss
Around 50 percent of uveitis cases are idiopathic: no underlying cause is ever found
The other 50 percent are associated with systemic autoimmune conditions, infections, or rarely malignancy
Uveitis is a relapsing-remitting condition for many patients: flares are treated aggressively and remission is maintained
Long-term use of corticosteroids, the mainstay of treatment, can cause cataracts and glaucoma that need monitoring

Most common type Anterior Around 75 percent of uveitis cases affect the front of the eye

Idiopathic cases ~50% Of uveitis cases have no identifiable underlying cause

Working-age impact No. 3 Cause of preventable blindness in working-age adults

What Happens Inside the Eye

Side-by-side cross-section comparing a normal eye on the left with clear anterior chamber and vitreous, versus an inflamed eye on the right showing anterior uveitis with cells in the anterior chamber, hypopyon, thickened iris, and vitreous haze — Left: a normal eye. Right: uveitis with inflammatory cells in the anterior chamber, hypopyon at the bottom, and vitreous haze.

Uveitis occurs when the immune system, for reasons that are often unclear, mounts an inflammatory response within the eye. White blood cells enter the eye through the blood vessels of the uveal tract and accumulate in the aqueous humour of the anterior chamber (cells and flare), the vitreous (vitritis), and the retina and choroid (chorioretinitis). These cells are visible to the ophthalmologist at the slit lamp and on OCT, and their density is used to grade the severity of the inflammation and monitor the response to treatment.

Left untreated, the consequences accumulate. Inflammatory cells damage the trabecular meshwork and cause raised intraocular pressure. The iris can adhere to the lens (posterior synechiae) or to the cornea (anterior synechiae), distorting the pupil and blocking drainage. Chronic cystoid macular edema from posterior inflammation thickens the central retina and blurs vision. Cataracts develop, both from the inflammation itself and from the steroids used to treat it. Band keratopathy deposits calcium in the cornea. Each of these is a complication that early and effective treatment aims to prevent.

The Clinical Signs of Anterior Uveitis

Hyperrealistic close-up of an eye with severe anterior uveitis showing circumcorneal injection with intense redness at the limbus, a yellowish hypopyon layer of inflammatory cells settled at the bottom of the anterior chamber, keratic precipitates as deposits on the inner corneal surface, and an irregular pupil from posterior synechiae where the iris has adhered to the lens — Severe anterior uveitis: circumlimbal redness, hypopyon (yellow cell layer at the bottom of the anterior chamber), keratic precipitates on the cornea, and an irregular pupil from synechiae.

The image above shows four simultaneous signs in one eye. Circumcorneal injection: the redness is most intense at the limbus, the junction between the cornea and the white of the eye, fading toward the periphery. This pattern distinguishes uveitis from conjunctivitis, where redness is more diffuse. Hypopyon: the yellowish layer settled at the bottom of the iris is a gravity-dependent collection of white cells in the anterior chamber, visible to the naked eye in severe cases. Keratic precipitates: the deposits on the inner corneal surface are clumps of inflammatory cells and protein. Synechiae: the irregular pupil margin shows where the iris has stuck to the lens behind it.

Types of Uveitis

Anterior uveitis

The most common form, accounting for around 75 percent of cases. Inflammation is confined to the iris and ciliary body. Presents with pain, redness, photophobia, and blurred vision. Often unilateral and acute in onset. HLA-B27 positive individuals, who have an underlying tendency to inflammatory conditions including ankylosing spondylitis, reactive arthritis, and inflammatory bowel disease, are particularly prone to recurrent acute anterior uveitis. Most cases respond well to topical steroid drops and dilating drops to prevent synechiae.

Intermediate uveitis

Inflammation centered on the pars plana and the peripheral vitreous. Often presents more insidiously with floaters and blurred vision rather than acute pain and redness. Associated with multiple sclerosis, sarcoidosis, and in younger patients with pars planitis, an idiopathic form. Snowbanking (white inflammatory exudate over the pars plana) and snowball opacities in the vitreous are characteristic on examination. Cystoid macular edema is the main cause of vision loss and responds to periocular or systemic steroid treatment.

Posterior uveitis

Inflammation of the choroid and retina. The most visually threatening form because it directly involves the tissue responsible for vision. Causes include toxoplasmosis (the most common infectious cause of posterior uveitis worldwide), cytomegalovirus retinitis in immunocompromised patients, sarcoidosis, Behcet’s disease, and Vogt-Koyanagi-Harada syndrome. Symptoms are floaters and visual loss without significant pain. Fundus examination reveals white infiltrates, retinal vasculitis, and vitreous haze. Treatment depends entirely on identifying the cause: infectious uveitis requires antimicrobial treatment before or alongside immunosuppression.

Panuveitis

Inflammation involving all three anatomical zones simultaneously. Always demands a thorough systemic workup to identify an underlying cause. Sarcoidosis, Behcet’s disease, Vogt-Koyanagi-Harada syndrome, and sympathetic ophthalmia (following penetrating trauma to the fellow eye) are among the causes. The visual prognosis is more guarded and treatment typically requires systemic immunosuppression.

Causes and Investigation

Around 50 percent of uveitis cases are idiopathic. For the other half, a systematic workup guides treatment. Investigations typically include:

Blood tests: FBC, ESR, CRP, ACE (sarcoidosis), HLA-B27, syphilis serology, toxoplasma antibodies, ANA, ANCA
Chest X-ray or CT: sarcoidosis, tuberculosis
Tuberculin skin test or IGRA: TB-associated uveitis
Infectious serology depending on clinical pattern: herpes viruses, CMV, Lyme disease in endemic areas
MRI brain if multiple sclerosis or VKH is suspected
Fluorescein angiography and OCT to characterise retinal involvement and macular edema

In practice, a positive result on investigation changes management in only a minority of cases, but missing a treatable infectious cause or a systemic disease that needs treatment in its own right is the main reason to investigate thoroughly.

Treatment

Corticosteroids

The foundation of uveitis treatment. Topical prednisolone drops hourly during an acute flare of anterior uveitis, tapering slowly as the inflammation settles. Periocular steroid injections (subconjunctival or sub-Tenon’s) provide sustained local delivery for intermediate and posterior uveitis. Oral prednisolone for severe or bilateral disease. Intravitreal dexamethasone implants for chronic uveitic macular edema. The challenge is that steroids cause cataracts and raised intraocular pressure with chronic use, both of which need monitoring at every visit.

Dilating drops

Cyclopentolate or atropine drops are used in acute anterior uveitis to keep the pupil dilated, which prevents the iris from adhering to the lens and breaks down any early synechiae that have formed. They also reduce the pain of ciliary spasm. Patients find the blurred vision and light sensitivity from dilation inconvenient, but the alternative, a permanently irregular pupil with posterior synechiae, is far worse.

Immunosuppressive agents

For patients with chronic uveitis requiring long-term treatment, steroid-sparing immunosuppressive agents are introduced to reduce the steroid burden. Methotrexate, mycophenolate mofetil, and azathioprine are the most commonly used. They take weeks to months to reach full effect and require blood test monitoring. Biologic agents, particularly adalimumab (Humira), are approved for non-infectious uveitis that has not responded to conventional immunosuppression and have good evidence for maintaining remission.

Treating the underlying cause

Infectious uveitis requires specific antimicrobial treatment: pyrimethamine and sulfadiazine for toxoplasmosis, antivirals for herpetic uveitis, antifungals for fungal endophthalmitis. Steroids without antimicrobial cover in infectious uveitis can cause catastrophic worsening. This is why the distinction between infectious and non-infectious uveitis is the most important diagnostic step in the whole workup.

Uveitis and Systemic Disease: The Bigger Picture

For many patients, uveitis is the first sign of a systemic inflammatory condition they did not know they had. HLA-B27 positive patients presenting with recurrent acute anterior uveitis often have or will develop ankylosing spondylitis, reactive arthritis, psoriatic arthritis, or inflammatory bowel disease. A rheumatology referral is appropriate when HLA-B27 positivity is confirmed, even without current systemic symptoms.

Sarcoidosis is a common cause of granulomatous uveitis and can affect the lungs, skin, lymph nodes, and nervous system as well as the eyes. A patient with bilateral chronic granulomatous uveitis and no systemic diagnosis warrants thorough investigation for sarcoidosis even when chest X-ray is normal, as CT chest is more sensitive.

Behcet’s disease, a vasculitis causing oral and genital ulcers alongside ocular inflammation, is predominantly found in patients from Turkey, the Middle East, and East Asia, and causes one of the most aggressive forms of panuveitis. Early recognition and aggressive immunosuppression, including biologic therapy, are needed to prevent severe vision loss.

Seek Same-Day Assessment If You Have

A red, painful, photophobic eye, particularly if you have had uveitis before
Sudden floaters or visual loss in a patient with known uveitis
A known uveitis patient on immunosuppression who develops any new ocular symptom
Eye pain and redness in an immunocompromised patient, including those on biologics or after transplant

Uveitis flares treated early do less damage than flares allowed to smolder. A patient who knows their uveitis pattern and recognises a flare starting should not wait for a routine appointment: same-day contact with the uveitis service is appropriate. In immunocompromised patients, infectious uveitis including endophthalmitis can deteriorate rapidly and requires urgent assessment regardless of whether the eye looks typical for their usual pattern.

Frequently Asked Questions About Uveitis

Why does my uveitis keep coming back?
For most patients, uveitis is a chronic relapsing condition, not a single event. That’s the honest answer to why it keeps coming back. The underlying autoimmune or inflammatory drive does not disappear after a flare is treated; it quietens temporarily. Triggers vary between patients: stress, intercurrent infections, and changes in systemic medication can all provoke a flare. Long-term maintenance immunosuppression aims to reduce the frequency and severity of relapses, but it does not eliminate them entirely in every case.
Will I go blind from uveitis?
Most people with well-managed uveitis don’t. The risk is real — it’s one of the leading causes of preventable blindness in working-age adults — but it is largely preventable with the right treatment and monitoring. The patients at greatest risk of severe vision loss are those with posterior or panuveitis, those with repeated or prolonged flares, those who present late, and those who are poorly adherent to treatment. Anterior uveitis, the most common form, rarely causes blindness when treated appropriately.
Can the steroid drops cause damage to my eyes?
Yes, with long-term use. Topical corticosteroids raise intraocular pressure in a proportion of patients (steroid responders), which if undetected can cause glaucomatous optic nerve damage. They also accelerate cataract formation with prolonged use. Both are manageable: intraocular pressure is checked at every uveitis visit, and when raised, pressure-lowering drops are added. Steroid-sparing agents are introduced for patients requiring long-term treatment to reduce cumulative steroid exposure. Knowing the risks is not a reason to avoid treatment: untreated uveitis causes far more damage than treated uveitis.
I have been told I have HLA-B27 positive uveitis. What does that mean for my joints?
HLA-B27 is a genetic marker associated with a group of inflammatory conditions called spondyloarthropathies, including ankylosing spondylitis, reactive arthritis, and psoriatic arthritis. Having HLA-B27 positive uveitis means you are at a much higher risk of developing one of these conditions if you haven’t already. Back pain or stiffness, particularly morning stiffness lasting more than 30 minutes, swollen joints, or skin and bowel symptoms should prompt a rheumatology referral. Treating the systemic condition often improves the uveitis frequency as well.
Are there foods or lifestyle changes that help uveitis?
No dietary intervention has strong evidence for reducing uveitis activity specifically. General measures that support immune regulation, adequate sleep, stress management, not smoking, and a diet rich in anti-inflammatory foods, are sensible but should not be presented as substitutes for medication during active disease. Some patients with uveitis associated with inflammatory bowel disease find that gut flares and eye flares are linked, and that managing the bowel condition stabilises the eyes.
My child has been diagnosed with uveitis but has no symptoms. Is that normal?
Yes. And it is one of the most important things to know about childhood uveitis associated with juvenile idiopathic arthritis (JIA). Completely asymptomatic, no red eye, no pain — but damaging if not caught. JIA-associated uveitis is typically completely asymptomatic: the eye is white, not red or painful. Children with JIA, particularly those who are ANA positive and female, require regular slit lamp screening even with no eye symptoms because they can develop severe uveitis that causes significant damage before anyone notices anything is wrong. This is why ophthalmology review schedules for JIA children are not optional and should not be deferred.

If you would like to learn more, the NHS uveitis page and the American Academy of Ophthalmology’s uveitis page offer additional patient-friendly information about symptoms, causes, and treatment.