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. Specialist care is provided by the uveitis and inflammation subspecialty page.
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, including secondary glaucoma
- 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
What Happens Inside the Eye
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
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
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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.
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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.
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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.
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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.
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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.
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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.
Uveitis is inflammation of the uveal tract , the iris, ciliary body, and choroid , but the term encompasses a broader set of intraocular inflammatory conditions including involvement of the retina, vitreous, and optic nerve. It is anatomically classified into anterior, intermediate, posterior, and panuveitis based on the primary site of inflammation. This classification is clinically fundamental because it determines the likely causes, investigation pathways, treatment approach, and complication profile. Uveitis accounts for approximately 10-15% of legal blindness in working-age adults in high-income countries, disproportionate to its overall prevalence. The majority of anterior uveitis is idiopathic or HLA-B27-associated; posterior and panuveitis require a more extensive systemic and infective workup. The cornerstone of acute anterior uveitis management is topical corticosteroid, with cycloplegia for pain and posterior synechiae prevention.
Clinical Overview: Uveitis
- Anatomical classification: Anterior uveitis (iritis, iridocyclitis) , AC cells and flare; Intermediate uveitis , vitreous cells, snowballs, snowbanking; Posterior uveitis , chorioretinitis, retinitis, papillitis; Panuveitis , all segments
- Anterior uveitis first-line: Topical corticosteroid (prednisolone acetate 1% hourly-2-hourly in acute phase, taper over 4-8 weeks); cyclopentolate 1% or atropine 1% (cycloplegia for pain + prevents posterior synechiae)
- Grading: SUN (Standardization of Uveitis Nomenclature) working group cell grades: 0 (none), 0.5+ (1-5 cells), 1+ (6-15), 2+ (16-25), 3+ (26-50), 4+ (>50 cells per 1mm² field at 1mm slit beam)
- HLA-B27 association: Present in ~50% of acute anterior uveitis. Associated systemic conditions: ankylosing spondylitis, reactive arthritis, psoriatic arthritis, IBD-associated arthritis. Ask about back pain, joint swelling, skin rashes, bowel symptoms.
- Posterior/panuveitis workup: FBC, ESR, CRP, ACE (sarcoidosis), chest X-ray (sarcoidosis, TB), syphilis serology (VDRL/TPPA), toxoplasma IgG/IgM, HIV, TB (Quantiferon/IGRA). Extend if indicated: ANA, ANCA, HLA-B27, Lyme serology, HSV/VZV/CMV PCR from AC tap
- Complications requiring monitoring: Posterior synechiae, cataract (steroid-induced and inflammatory), raised IOP (steroid-response and angle involvement), cystoid macular edema (CME), optic disc swelling, band keratopathy (chronic anterior uveitis)
Pathophysiology and Classification
Uveitis results from immune-mediated tissue damage , either as part of a recognized systemic inflammatory condition, as an immune response to an infectious agent within the eye, or as an isolated ocular autoimmune process. The distinction between infectious and non-infectious uveitis is clinically critical because immunosuppression (the treatment for non-infectious uveitis) can dramatically worsen infectious uveitis.
Anterior uveitis: Predominantly a T-cell-mediated process targeting uveal antigens. In HLA-B27-associated disease, molecular mimicry between bacterial antigens (particularly Klebsiella in ankylosing spondylitis) and HLA-B27 peptides is the proposed mechanism. Acute anterior uveitis (AAU) is typically unilateral, acute in onset, and alternating between eyes in HLA-B27-positive patients. Granulomatous anterior uveitis (mutton-fat keratic precipitates [KPs], iris nodules) suggests sarcoidosis, tuberculosis, or sympathetic ophthalmia.
Intermediate uveitis: Predominantly involves the pars plana and anterior vitreous. The most common cause in younger patients is idiopathic (pars planitis). Multiple sclerosis is the most important systemic association and must be considered in any intermediate uveitis, particularly in young women. Sarcoidosis, Lyme disease, and rarely lymphoma should also be excluded.
Posterior and panuveitis causes by frequency: Toxoplasma retinochoroiditis (the most common infectious cause globally), CMV retinitis (in immunocompromised patients), viral retinitis (ARN , acute retinal necrosis , from HSV/VZV), syphilitic chorioretinitis, TB, sarcoidosis, Behcet’s disease, Vogt-Koyanagi-Harada (VKH) syndrome, sympathetic ophthalmia, birdshot retinochoroidopathy, and multifocal choroiditis.
Examination and Grading
Anterior segment: Ciliary flush (limbal injection), corneal KPs (fine/stellate = non-granulomatous; large/mutton-fat = granulomatous), anterior chamber cells and flare graded by SUN criteria, posterior synechiae (iris adhesions to anterior lens surface), iris nodules (Busacca = stroma; Koeppe = pupil margin), lens changes. IOP: typically low in acute anterior uveitis from reduced aqueous production; elevated IOP suggests trabecular inflammation or angle involvement.
Posterior segment: Vitreous cells and haze (graded 0-4+), snowballs (inferior vitreous aggregates in intermediate uveitis), snowbanking (pars plana exudates), chorioretinal lesions (active: white/yellow, fluffy edges; inactive: pigmented scars), retinal vasculitis (perivenular sheathing, occlusion), disc swelling, CME (best confirmed on OCT).
Investigation Strategy
First episode of unilateral acute non-granulomatous anterior uveitis: HLA-B27 and a directed systemic history (back pain, joint symptoms, bowel disease, skin rashes) is sufficient for most first presentations in a young-to-middle-aged adult. No further laboratory workup is required unless the history suggests a specific systemic condition or the uveitis fails to respond to treatment.
Bilateral, granulomatous, recurrent, or posterior/panuveitis: Broad workup required. Minimum: FBC, ESR, CRP, serum ACE and lysozyme (sarcoidosis), syphilis serology (VDRL/RPR + confirmatory TPPA/FTA-abs), toxoplasma IgG/IgM, HIV, chest X-ray. Extend as indicated: Quantiferon-TB Gold (IGRA) or Mantoux for TB, ANA/ANCA for connective tissue disease, HLA-B51 for Behcet’s, HLA-A29 for birdshot.
Aqueous tap (anterior chamber paracentesis): For atypical presentations, suspected viral uveitis (Posner-Schlossman syndrome, CMV-related Posner-Schlossman, herpes), or immunocompromised patients. PCR analysis of aqueous for HSV, VZV, CMV, toxoplasma, and other organisms provides a specific diagnosis. A 30-gauge needle paracentesis at the slit lamp is a relatively low-risk procedure in experienced hands and changes management in approximately 30-40% of cases in selected populations.
Medical Management
Topical corticosteroid: Prednisolone acetate 1% (most potent topical steroid in common use; shaken before use as a suspension). Acute AAU: start hourly dosing, taper over 4-8 weeks guided by cell response. Do not taper too quickly , recurrence from premature steroid withdrawal is the most common cause of treatment failure. Dexamethasone 0.1% is an alternative with slightly lower IOP-raising potential.
Cycloplegia: Cyclopentolate 1% twice-daily (shorter-acting, adequate for most AAU); atropine 1% twice-daily for more severe inflammation or to break posterior synechiae. Prevents synechiae by keeping the pupil mobile and relieves ciliary spasm pain. Do not omit cycloplegia , it is as important as the steroid in acute anterior uveitis.
Periocular and intraocular steroids: Sub-Tenon triamcinolone acetonide (40 mg/1 mL) for posterior uveitis, intermediate uveitis, or refractory CME. Intravitreal triamcinolone (4 mg/0.1 mL) or dexamethasone implant (Ozurdex 0.7 mg) for refractory posterior uveitis or CME. Monitor IOP carefully , steroid-responders develop significant IOP elevation (defined as IOP above 10 mmHg from baseline or above 21 mmHg).
Systemic immunosuppression: Required for chronic, bilateral, posterior, or recurrent uveitis causing ongoing inflammation despite topical treatment. Oral prednisolone: induction phase (1 mg/kg/day, max 80 mg), taper over weeks to the lowest controlling dose. Steroid-sparing agents for maintenance: methotrexate (7.5-25 mg weekly , favored in sarcoidosis, JIA-associated uveitis), mycophenolate mofetil (500 mg-1.5 g twice daily , favored in posterior uveitis and panuveitis), azathioprine (2-2.5 mg/kg/day). Anti-TNF biologics (adalimumab , VISUAL I and II trials: significantly reduces relapses in non-infectious uveitis , complementing the management of retinal vein occlusion-related uveitic complications): approved in EU and USA for non-infectious posterior and panuveitis. Reserved for steroid-sparing agent failures or JIA-associated uveitis in children.
Complications and Their Management
CME (cystoid macular edema): The primary cause of permanent vision loss in uveitis. Diagnosed on OCT (intraretinal cysts, elevated CST). Treat the underlying inflammation first. Adjunctive: topical NSAIDs (ketorolac, nepafenac), sub-Tenon or intravitreal triamcinolone, dexamethasone implant, or intravitreal anti-VEGF in selected cases. Chronic CME causes photoreceptor loss and lamellar hole formation , do not allow it to persist undertreated.
Raised IOP: Multifactorial in uveitis: trabecular inflammation (blocks drainage), posterior synechiae with pupil block and secondary angle closure, steroid response, anterior chamber angle damage from longstanding inflammation, neovascular glaucoma from ischemic retinal disease. Management: topical IOP-lowering drops (avoid PGAs in active uveitis , prostaglandins can exacerbate inflammation). Definitive: control the inflammation. Surgical IOP management (trabeculectomy or tube implant) for refractory uveitic glaucoma.
Posterior synechiae: Iris adhesions to the anterior lens surface. Prevented by adequate cycloplegia in acute uveitis. Once formed, phenylephrine 2.5% + cyclopentolate 1% alternating at 5-minute intervals (maximum 3 doses each) can break fresh synechiae. Long-standing synechiae are not reliably broken medically , surgical synechiolysis at time of cataract surgery may be required.
Clinical Decision Points
- Acute anterior uveitis, IOP elevated above 35 mmHg at presentation: This is not typical of straightforward inflammation-induced hypotony. Consider: Posner-Schlossman syndrome (CMV or HSV-related hypertensive iridocyclitis), acute angle-closure complicating uveitis, extensive trabecular inflammation. Aqueous tap for CMV/HSV PCR in Posner-Schlossman pattern (recurrent, mild anterior uveitis, markedly elevated IOP). CMV anterior uveitis requires valganciclovir, not standard uveitis treatment.
- Granulomatous anterior uveitis, negative sarcoidosis workup: Consider TB (IGRA, chest CT), syphilis (re-check serology), sympathetic ophthalmia (prior eye surgery or trauma history), VKH (look for associated dermatological and CNS features). Granulomatous pattern without a cause found after full workup warrants ocular oncology referral to exclude masquerade syndrome (primary intraocular lymphoma).
- Posterior uveitis, HIV-positive patient: CMV retinitis until proven otherwise. The appearance (pizza-pie fundus with hemorrhages and white retinal necrosis) is distinctive. Systemic ganciclovir or valganciclovir urgently. Do not use systemic corticosteroids without antiviral cover.
- Young woman with bilateral intermediate uveitis: MRI brain and orbits with contrast , MS is the most important diagnosis to exclude. If optic neuritis develops concurrently, this becomes urgent.
- Child with JIA on methotrexate, referred for uveitis: JIA-associated uveitis is typically insidious, non-red, and detected only at slit lamp. The absence of symptoms does not mean no inflammation , JIA children require regular slit-lamp examination regardless of symptoms. Adalimumab is approved for JIA-associated uveitis refractory to methotrexate.
Same-Day Assessment Required
- Acute red painful photophobic eye with significantly reduced VA , presumed anterior uveitis until proven otherwise; requires slit-lamp grading and IOP measurement same day
- Any immunocompromised patient with new floaters or visual symptoms , exclude CMV retinitis or other opportunistic retinal infection
- Acute retinal necrosis (ARN) , rapidly progressive peripheral necrotizing retinitis from HSV or VZV, causing RD in majority if untreated. Acute visual symptoms in any patient with prior herpetic disease: same-day ophthalmology and urgent IV aciclovir
- Bilateral simultaneous acute red eyes with systemic features (headache, tinnitus, vitiligo, skin changes) , VKH syndrome, requires urgent systemic steroid
Acute retinal necrosis (ARN) is one of the most rapidly destructive conditions in ophthalmology. Without urgent antiviral treatment (IV aciclovir 10-15 mg/kg TDS for 5-10 days followed by oral valaciclovir), retinal detachment , which is notoriously difficult to repair in ARN because of extensive retinal necrosis , develops in over 50% of cases. Speed of diagnosis and treatment directly determines the retinal outcome.
Clinical Pearls: Uveitis
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Syphilis can cause any pattern of uveitis. Test for it in every atypical, bilateral, or posterior uveitis.
Syphilitic uveitis is called “the great masquerader” because it can produce anterior, intermediate, posterior, or panuveitis; unilateral or bilateral; granulomatous or non-granulomatous; with any combination of retinal vasculitis, chorioretinitis, disc swelling, and CME. The seroprevalence of syphilis is rising in most countries. Syphilis serology (VDRL/RPR for activity, TPPA/FTA-abs for confirmation) should be checked in every atypical or bilateral uveitis , not just posterior presentations. Treatment with IV benzylpenicillin G is curative if initiated before structural damage.
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Stopping topical steroids too early is the most common cause of anterior uveitis recurrence. Taper slowly.
Patients frequently self-reduce or stop their prednisolone acetate drops once the eye looks and feels better. The absence of symptoms does not mean the inflammation has resolved , low-grade AC cells can persist and trigger a rebound flare when steroids are withdrawn. The standard taper is: every hour for 1 week, then every 2 hours, then every 4 hours, then QDS, then BD, then once daily, then alternate days , each step over at least a week, with slit-lamp confirmation of cell clearance before stepping down. Patients who reliably taper too quickly need a written drop schedule and explicit instructions.
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Primary intraocular lymphoma (PIOL) masquerades as posterior uveitis. Suspect it in patients over 50 with posterior uveitis not responding to immunosuppression.
PIOL (usually diffuse large B-cell lymphoma of the vitreoretinal compartment) typically presents as bilateral posterior uveitis with vitreous cells and yellowish subretinal infiltrates in adults over 50. It is frequently misdiagnosed and treated as idiopathic non-infectious uveitis, sometimes for years. It responds partially to steroids, which creates a false sense of improvement. Clinical clues: age over 50, bilateral vitreous cells, sub-RPE deposits (leopard-spot appearance), poor response to systemic steroids, concurrent or subsequent CNS lymphoma. Diagnostic aqueous or vitreous tap for cytology and IL-10:IL-6 ratio (elevated IL-10 suggests PIOL). Prognosis is poor without diagnosis.
Further reading: AAO Preferred Practice Pattern , Uveitis. For the uveitis-glaucoma overlap see glaucoma. The broader inflammation context is covered on the uveitis and inflammation subspecialty page.