Presentation

Acute: unilateral (usually) eye pain, photophobia, redness (ciliary flush), blurred vision, and tearing, developing over hours to days.
Chronic/recurrent forms (more often bilateral, notably in JIA-associated disease) can be relatively asymptomatic — a "white eye" uveitis found on routine screening.
Ask about systemic symptoms: low-back pain/stiffness (ankylosing spondylitis), joint pain (reactive arthritis, psoriatic arthritis), GI symptoms (IBD), skin/nail changes (psoriasis), genitourinary symptoms (reactive arthritis), and a history of cold sores or shingles (herpetic uveitis).

Findings

★ Signature Finding

Cells and flare in the anterior chamber on slit-lamp exam — the defining feature per the Standardization of Uveitis Nomenclature (SUN) criteria. Mechanism: breakdown of the blood-aqueous barrier allows inflammatory cells and protein into the aqueous humour.

Ciliary flush, keratic precipitates on the corneal endothelium (fine in most forms; large "mutton-fat" precipitates in granulomatous disease such as sarcoidosis), posterior synechiae, and miosis.
HLA-B27-associated disease: classically shows a fibrinous or even hypopyon reaction with rapid, severe onset, often recurrent and alternating between eyes.
IOP is commonly low during active inflammation (reduced ciliary body aqueous production), though secondary glaucoma can occur from trabeculitis, synechiae, or a corticosteroid response.

Etiology & Mechanism

Idiopathic in a substantial proportion of cases.
HLA-B27-associated: accounts for roughly half of acute anterior uveitis cases, linked to the spondyloarthropathies — ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and IBD-associated arthritis.
Infectious causes: herpes simplex virus and varicella zoster virus (often with elevated IOP during active disease and sectoral iris atrophy), syphilis, and tuberculosis.
Other systemic associations: sarcoidosis (typically granulomatous), juvenile idiopathic arthritis (chronic, often asymptomatic "white" uveitis in children — routine screening is essential), Behçet disease, and TINU syndrome.
Traumatic and drug-induced causes (e.g., rifabutin, cidofovir, bisphosphonates) also occur.

Red Flags — Do Not Miss

Critical — Do Not Miss

Hypopyon — suggests severe inflammation (HLA-B27 disease, Behçet disease) or an infectious process including endophthalmitis; requires prompt escalation of therapy and consideration of an infectious workup.
Elevated IOP in the setting of anterior uveitis — consider a herpetic aetiology (HSV/VZV) or secondary inflammatory glaucoma; herpetic disease requires targeted antiviral treatment, not anti-inflammatory therapy alone.
Uveitis in a child, especially a minimally symptomatic "quiet" white eye — screen for JIA-associated uveitis, which can silently cause band keratopathy, cataract, and glaucoma.
Poor response to standard topical corticosteroid therapy, or atypical features (granulomatous KPs, posterior segment involvement) — broaden the workup for infectious or systemic causes.

Investigations

Directed by the presentation and recurrence pattern rather than applied reflexively to every first, unilateral, non-granulomatous episode with an obvious precipitant.
For recurrent, bilateral, granulomatous, or atypical presentations: HLA-B27 testing; chest X-ray or CT (sarcoidosis, TB); RPR/FTA-ABS (syphilis); serum ACE and lysozyme (sarcoidosis); PPD or IGRA (TB); ANA (particularly in children).
Dilated fundus exam to exclude an intermediate/posterior/panuveitis component.

Management

Identify and treat any underlying cause when found — e.g., antiviral therapy for herpetic uveitis, or systemic disease-directed treatment in coordination with rheumatology/infectious disease.
Educate the patient about the high recurrence risk, particularly for HLA-B27-associated disease, and about seeking prompt care for future flares.

Treatment

First line: topical corticosteroids (e.g., prednisolone acetate 1% or difluprednate 0.05%), dosed intensively at first (up to hourly in severe cases) and then tapered slowly over weeks based on the degree of inflammation.
Cycloplegic/mydriatic agents (e.g., cyclopentolate or homatropine) for pain relief (via relief of ciliary spasm) and to prevent or break posterior synechiae.
Escalation for severe or steroid-refractory disease: periocular or intraocular corticosteroid injection, oral corticosteroids (~1 mg/kg as a commonly cited starting dose), or systemic immunosuppressive therapy.
Antiviral therapy (topical and/or oral) as primary treatment when a herpetic aetiology is confirmed or strongly suspected.

Follow-up

Close early follow-up (days to about a week) to confirm improving inflammation and to adjust the steroid taper — tapering too quickly risks a rebound flare; tapering too slowly risks steroid-induced glaucoma or cataract.
Monitor IOP closely during corticosteroid treatment for a steroid response.
Long-term monitoring for complications: posterior synechiae, cataract, glaucoma, cystoid macular oedema, and band keratopathy in chronic disease.
Children at risk for JIA-associated uveitis require scheduled screening exams at published surveillance intervals regardless of symptoms.

Clinical Pearl

💡 Clinical Pearl

Roughly half of acute anterior uveitis cases are associated with HLA-B27; although permanent vision loss is uncommon with adequate treatment, patients deserve counselling about the high recurrence risk and the possible underlying spondyloarthropathy that may not yet be diagnosed.

Differential Diagnoses

Condition	Key Distinguishing Point
Acute angle-closure glaucoma	Very high IOP (versus low/normal in uveitis), mid-dilated fixed pupil (versus often miotic in uveitis), corneal oedema.
Conjunctivitis	Prominent discharge, no cells/flare in the anterior chamber, usually painless or mildly irritating rather than photophobic.
Scleritis	Severe boring pain, often worse at night, globe tenderness to palpation, engorged scleral/episcleral vessels.
Corneal disease (keratitis/abrasion)	Fluorescein-positive epithelial defect, foreign-body sensation, typically a normal anterior chamber reaction unless secondary uveitis develops.
Intraocular tumour (masquerade syndrome)	Should be considered in atypical, steroid-resistant, or unilateral "uveitis," particularly in older or paediatric patients.

Pupilla

Anterior Uveitis