The uvea is the eye's middle layer — sandwiched between the outer coat (sclera and cornea) and the inner retina. It is profoundly vascular: the uveal vessels supply nutrition to the outer two-thirds of the retina, the lens, the ciliary body, and the iris. This vascularity is precisely what makes it vulnerable to systemic inflammatory disease. Any bloodborne pathogen, immune complex, or activated T-cell circulating in the body has direct access to the uveal tissue.

The uvea's three components produce three functionally distinct syndromes when inflamed: the iris and ciliary body (anterior uvea) produce the classic painful red eye with photophobia; the pars plana and vitreous base (intermediate zone) produce floaters and decreased vision with minimal pain; and the choroid (posterior uvea) produces vision loss through direct retinal and macular involvement — often entirely painless.

The mechanism of inflammation varies by aetiology — infectious uveitis involves direct microbial invasion or immune response to pathogen antigens deposited in uveal tissue; non-infectious uveitis involves T-cell mediated autoimmune attack on uveal or cross-reactive antigens. In HLA-B27-associated uveitis, molecular mimicry between bacterial antigens and self-peptides presented by the HLA-B27 molecule is the leading hypothesis. In TB uveitis, the mycobacterial antigens provoke a delayed-type hypersensitivity response in sensitised individuals — frequently without active TB elsewhere.

The global prevalence of uveitis is approximately 115 per 100,000 population. India's figures are substantially higher — driven by a distinctive aetiological landscape shaped by the country's infectious disease burden.

Tuberculosis is the dominant factor. India carries 26% of the global TB burden — 2.8 million new cases annually. In Indian uveitis clinics, TB is the single most common identifiable cause, accounting for 15–30% of all cases in tertiary centre series (Biswas et al., Aravind Eye Care data, L.V. Prasad data). Critically, ocular TB rarely coincides with active pulmonary TB — in most patients, uveitis is the presenting feature of a latent or contained mycobacterial infection responding immunologically rather than microbiologically.

HLA-B27-associated uveitis is the second major category — accounting for 17–25% of anterior uveitis in India. HLA-B27 prevalence in the Indian population is 4–8%, with the antigen associated with ankylosing spondylitis, reactive arthritis (formerly Reiter syndrome), psoriatic arthritis, and inflammatory bowel disease. Patients may present with recurrent acute anterior uveitis years before a rheumatological diagnosis is established.

Viral uveitis — driven by HSV, VZV, and CMV — is increasingly recognised with wider access to PCR-based aqueous humour analysis. Toxoplasmosis remains the leading cause of posterior uveitis in many regions. Vogt-Koyanagi-Harada (VKH) syndrome — a bilateral panuveitis with meningitis, tinnitus, and skin depigmentation — is disproportionately common in pigmented races including Indian, Japanese, and Hispanic populations.

The Standardisation of Uveitis Nomenclature (SUN) Working Group classification — the global standard since 2005 — divides uveitis by the primary anatomical site of inflammation. This is not merely academic: the treatment approach, the associated systemic diseases, and the risk of complications differ substantially between types.

At the slit lamp, the ophthalmologist directs a narrow beam of light into the anterior chamber. In a normal eye, the aqueous humor is optically clear — the beam passes through invisibly. In uveitis, inflammatory cells and protein leak from iris vessels into the aqueous. The beam becomes visible as a bright shaft — the Tyndall effect — with individual cells visible as bright dots crossing the beam, and protein measured as "flare" (the hazy background glow). The SUN Working Group standardises cell grading as follows:

The single most important decision in uveitis management is determining whether the inflammation is infectious (requiring specific antimicrobial treatment) or non-infectious (requiring immunosuppression). Giving steroids to an undiagnosed infectious uveitis — particularly CMV or HSV — can be catastrophic. Conversely, withholding steroids from a non-infectious panuveitis allows irreversible structural damage to accumulate.

Uveitis diagnosis proceeds in two parallel tracks: the ophthalmic assessment (establishing location, grade, morphology, and structural complications) and the systemic workup (identifying the underlying aetiology to guide targeted treatment). Neither is sufficient alone.

• Slit-lamp examination: Cell and flare grading in the anterior chamber. KP morphology — fine (non-granulomatous, e.g. HLA-B27) vs mutton-fat (granulomatous, e.g. TB, sarcoidosis). Posterior synechiae. Iris nodules (Busacca = iris stroma; Koeppe = pupil margin). Corneal oedema. IOP (uveitis can both lower and raise IOP depending on mechanism).
• Dilated fundoscopy: Vitreous cells and haze, snowballs (intermediate uveitis), retinal or choroidal lesions, vasculitis, disc oedema, macular oedema, retinal detachment.
• OCT macula: Cystoid macular oedema (CMO) is the primary cause of visual loss in uveitis. OCT quantifies CMO and monitors treatment response. Also detects subretinal fluid in VKH (characteristic "waves" of choroidal thickening).
• Fluorescein angiography (FA): Maps retinal vasculitis (vessel leakage, staining), CNV, non-perfusion. ICG angiography visualises choroidal disease better than FA.
• B-scan ultrasound: When media opacity prevents fundal view — identifies posterior vitreous detachment, retinal detachment, choroidal thickening (VKH), and choroidal mass.
• Aqueous humour PCR: Paracentesis with PCR for HSV, VZV, CMV, toxoplasma, TB in selected cases — highest diagnostic yield for infectious uveitis when systemic workup is inconclusive.

• TB: Mantoux (TST), IGRA (QuantiFERON-TB Gold) — preferred as BCG vaccination does not cause false positives. Chest X-ray and HRCT chest. ADA levels in selected cases.
• HLA-B27: Typed in all anterior uveitis — guides rheumatology referral if positive. Sacroiliac joint X-ray for ankylosing spondylitis in symptomatic patients.
• Viral: HSV/VZV/CMV serology (IgG/IgM). PCR on aqueous if herpetic aetiology strongly suspected.
• Sarcoidosis: ACE (angiotensin-converting enzyme), serum lysozyme, CXR, HRCT. Gallium scan or PET in selected cases.
• Autoimmune: ANA, dsDNA (lupus), ANCA (vasculitis), RF (RA).
• Toxoplasmosis: IgG and IgM serology (IgG positive in most adults; IgM suggests recent infection).
• FBC, ESR, CRP: Non-specific but guide systemic activity.
• VDRL/TPHA: Syphilis serology — syphilitic uveitis mimics almost every other form and is eminently treatable; never miss it.

Anterior uveitis is treated primarily with topical agents. Prednisolone acetate 1% eye drops — the gold standard topical steroid — suppress anterior chamber inflammation. Dosing is intensive initially (every 1–2 hours while awake in acute Grade 2+ uveitis), then tapered over weeks as cells clear. Dexamethasone 0.1% is an alternative. Cycloplegic agents (cyclopentolate 1%, atropine 1%) dilate the pupil, relieve ciliary spasm (the major source of pain), and break or prevent posterior synechiae — adhesions between the iris and anterior lens capsule that distort the pupil and impair aqueous flow.

Periocular steroid injections (sub-Tenon's triamcinolone acetonide) are used for refractory anterior uveitis or macular oedema not responding to topical therapy. Intravitreal implants (fluocinolone acetonide — Yutiq, Iluvien) provide sustained corticosteroid delivery for 18–36 months in chronic non-infectious uveitis.

Oral prednisolone (1 mg/kg/day, typically 40–80 mg/day) is the first-line for posterior and panuveitis, and for anterior uveitis that fails topical treatment. IV methylprednisolone (1g/day × 3 days) is used for acute VKH, severe bilateral posterior uveitis, or any sight-threatening inflammation requiring rapid suppression. Systemic steroids are never a long-term solution — the side effect profile (weight gain, diabetes, hypertension, osteoporosis, infection, adrenal suppression) mandates transition to steroid-sparing agents within 3–6 months.

• Methotrexate (7.5–25 mg/week oral or SC) — most commonly used; takes 3–6 months to reach full effect; requires folic acid supplementation and LFT monitoring.
• Mycophenolate mofetil (1–3 g/day) — effective for posterior uveitis and VKH; better GI tolerance than azathioprine in many patients.
• Azathioprine (1–3 mg/kg/day) — long-established; thiopurine methyltransferase (TPMT) testing recommended before initiation.
• Cyclosporine (2.5–5 mg/kg/day) — faster onset than antimetabolites; used for Behçet retinal vasculitis. Nephrotoxicity limits long-term use.

Adalimumab (Humira) — the first biologic with FDA approval specifically for non-infectious intermediate, posterior, and panuveitis in adults (2016) and children (2017). Anti-TNF-α mechanism; subcutaneous injection every 2 weeks. The VISUAL I and VISUAL II trials demonstrated significant reduction in treatment failure vs placebo. Available in India through the Adalimumab Biosimilar programme.

Infliximab — IV anti-TNF-α; preferred for Behçet uveitis in many centres. Rituximab (anti-CD20) for refractory cases. Secukinumab (IL-17 inhibitor) emerging evidence in HLA-B27 uveitis prevention.

• TB uveitis: Standard RNTCP regimen — 2HRZE/4HR (rifampicin, isoniazid, pyrazinamide, ethambutol × 2 months; then rifampicin + isoniazid × 4 months). Concurrent controlled corticosteroids to suppress the immune-mediated damage while antimicrobials clear the antigen load. Minimum 6 months; some guidelines recommend 9 months for ocular TB.
• Herpetic (HSV/VZV): Oral acyclovir (400–800 mg 5×/day) or valacyclovir (1 g TDS) for acute attack. IV acyclovir for ARN (acute retinal necrosis — ophthalmological emergency). Long-term suppressive therapy reduces recurrence.
• CMV uveitis: Oral valganciclovir (900 mg BD) for active disease. Intravitreal ganciclovir or foscarnet for retinitis. HAART optimisation in HIV-positive patients.
• Toxoplasmosis: Trimethoprim-sulfamethoxazole or classic triple therapy (pyrimethamine + sulfadiazine + folinic acid) for active lesions near the macula or optic disc; systemic steroids to reduce inflammatory damage.

The complications of uveitis are largely independent of the underlying cause — they are structural consequences of chronic intraocular inflammation. Each complication represents an escalating threat to vision.

• Uveitic glaucoma — the most common cause of permanent vision loss in uveitis. Mechanisms include trabecular meshwork inflammation and scarring, posterior synechiae causing pupillary block, steroid-induced IOP elevation, and neovascular glaucoma in ischaemic posterior uveitis. Uveitic glaucoma is notoriously difficult to control — often requiring multiple medications, trabeculectomy, or tube shunts. Full coverage in our Glaucoma guide.
• Complicated cataract — both the chronic inflammation and the steroid treatment required to control it cause posterior subcapsular cataract (PSC). PSC from chronic uveitis tends to be dense, visually significant, and forms faster than age-related nuclear cataract. Cataract surgery in uveitis requires careful timing — ideally after 3 months of quiescence — and meticulous perioperative inflammation control. See our Complete Cataract Surgery guide for the surgical principles; uveitic eyes require modified technique.
• Cystoid macular oedema (CMO) — fluid accumulation in the macular layers secondary to BRB breakdown by inflammatory mediators. The leading cause of permanent central vision loss in uveitis. Treated with periocular or intravitreal steroids, anti-VEGF agents, and systemic immunosuppression.
• Band keratopathy — calcium deposition in the superficial cornea, particularly in children with chronic anterior uveitis (JIA-associated). Causes visual obscuration and ocular discomfort.
• Posterior synechiae → seclusio pupillae → iris bombé — 360° posterior synechiae seal the pupil (seclusio pupillae), blocking aqueous flow from posterior to anterior chamber. The iris bulges forward (iris bombé), dramatically raising IOP. This is a surgical emergency — laser peripheral iridotomy (LPI) if iris is clear, or surgical iridectomy.
• Retinal detachment / vitreoretinal complications — chronic vitreous inflammation causes fibrovascular traction; posterior uveitis can cause exudative RD. See our Retinal Detachment guide.
• Phthisis bulbi — end-stage uveitis. The eye shrinks, loses all visual function, and ultimately atrophies from chronic hypotony and scarring. Prevention requires aggressive management of every earlier stage.