Uveitis

Uveitis: the red painful eye your GP must not miss

Uveitis is inflammation of the uveal tract — the iris, ciliary body, and choroid — inside the eye. Anterior uveitis (iritis) accounts for about 90% of cases and presents with a painful red eye, photophobia, and blurred vision.

The GP's job is to recognise it and arrange same-day ophthalmology review, not to treat it without specialist input. Untreated uveitis can cause permanent vision loss from cataracts, glaucoma, or retinal damage. Most anterior uveitis responds well to topical steroid eyedrops and a pupil-dilating agent when supervised by an ophthalmologist.

What is uveitis?

The uvea is the middle vascular layer of the eye — comprising the iris (front), the ciliary body (middle), and the choroid (back). When any part of this layer becomes inflamed, the condition is called uveitis. It is classified by location: anterior uveitis (iris and ciliary body — about 92% of cases), intermediate uveitis (vitreous and pars plana), posterior uveitis (retina and choroid), and panuveitis (all layers).

Anterior uveitis is also called iritis or iridocyclitis. It is the most common form in Australian general practice and typically presents as an acute painful red eye with photophobia and blurred vision. RANZCO and Therapeutic Guidelines (eTG) both classify this as a condition requiring same-day specialist ophthalmology review — it is not a condition GPs diagnose and treat independently without specialist oversight.

Uveitis affects people of all ages. Anterior uveitis incidence is approximately 17–25 per 100,000 per year in Australia. Untreated or poorly managed uveitis leads to synechiae (adhesions), cataracts, glaucoma, cystoid macular oedema, and permanent vision loss.

A. Core clinical — the AU general practice framework

Anatomic classification and the SUN system

The Standardisation of Uveitis Nomenclature (SUN) Working Group established the anatomic classification used worldwide:

ClassSiteCommon examples
Anterior (~92%)Iris ± ciliary bodyHLA-B27 acute anterior uveitis, iridocyclitis
IntermediateVitreous, pars planaPars planitis, MS-associated
PosteriorRetina, choroidToxoplasmic chorioretinitis, CMV retinitis
PanuveitisAll chambersBehçet’s disease, Vogt-Koyanagi-Harada (VKH), sarcoidosis

Course is described as acute (less than 3 months), recurrent (episodes with gap of 3 or more months), or chronic (persistent or returning within 3 months of stopping treatment).

Causes

Aetiology can be non-infectious or infectious:

Non-infectious (~70% of uveitis overall):

  • Idiopathic — the most common single category (~50% of all uveitis).
  • HLA-B27-associated spondyloarthropathies — ankylosing spondylitis, reactive arthritis, psoriatic arthritis, inflammatory bowel disease-related arthritis. Roughly 32% of acute anterior uveitis is HLA-B27-related, and these patients are at risk of recurrent episodes.
  • Systemic autoimmune conditions — sarcoidosis, juvenile idiopathic arthritis, multiple sclerosis, Behçet’s disease, VKH syndrome.
  • Drug-induced — immune checkpoint inhibitors (ipilimumab, nivolumab, pembrolizumab), rifabutin, bisphosphonates.

Infectious (~20%):

  • Herpes simplex virus (HSV) and varicella-zoster virus (VZV) — most common infectious causes of anterior uveitis.
  • Toxoplasma gondii — most common infectious cause of posterior uveitis worldwide.
  • Syphilis — must always be excluded in atypical or bilateral uveitis.
  • Tuberculosis, cytomegalovirus (in immunocompromised patients).

Recognising uveitis in general practice

Symptoms of anterior uveitis:

  • Aching, deep eye pain — often periorbital and worse in bright light.
  • Photophobia — typically prominent and the reason patients present.
  • Blurred vision — varies from mild to significant.
  • Redness — a “circumlimbal” (ciliary) injection around the corneal edge, not at the conjunctival periphery as in conjunctivitis.
  • Tears without discharge.

Examination findings available to a GP:

  • Visual acuity testing — documenting any reduction is clinically important.
  • Pupil assessment — an irregular or miotic (constricted) pupil suggests posterior synechiae have already formed.
  • Circumlimbal injection — the ring of redness concentrated at the corneal margin.
  • Absence of conjunctival discharge — uveitis does not produce a mucopurulent discharge.

Slit-lamp examination — the definitive tool for grading anterior chamber cells and flare — is performed by the ophthalmologist, not in general practice.

Must-not-miss differentials

Before diagnosing uveitis the following conditions must be considered:

ConditionKey discriminator
Acute angle-closure glaucomaSevere pain, halos around lights, fixed mid-dilated pupil, rock-hard eye — ophthalmic emergency, call ambulance
EndophthalmitisPost-surgical or post-penetrating eye — severe progressive inflammation — surgical emergency
Microbial keratitisContact lens wearer, corneal infiltrate, extreme photophobia — requires ophthalmology same day
ConjunctivitisDiffuse redness, discharge, minimal pain, vision normal — see [[red-eye]]
Episcleritis / scleritisSectoral redness (episcleritis mild and self-limiting), deep boring pain (scleritis — often autoimmune)
Subconjunctival haemorrhageBright red patch, painless, vision normal — self-resolving
Retinal artery occlusion (CRAO)Sudden painless vision loss, white retina with cherry-red spot — vascular emergency
Giant cell arteritisAge ≥50, jaw claudication, scalp tenderness, ESR markedly elevated — emergency for visual loss prevention

Investigations

eTG and RANZCO recommend a stepwise approach:

For a first attack of mild unilateral anterior uveitis in an otherwise healthy young adult: No extensive workup is required. Treat empirically and refer to ophthalmology. Most of these cases are idiopathic or HLA-B27-associated.

For recurrent, bilateral, posterior, or atypical uveitis — the following investigations are indicated:

  • HLA-B27 — if anterior uveitis with spinal or joint symptoms.
  • Syphilis serology (RPR and TPHA) — mandatory in all non-trivial uveitis presentations.
  • QuantiFERON-TB Gold — when tuberculosis is a realistic possibility.
  • ACE and serum calcium — for sarcoidosis.
  • HIV serology (with informed consent) — especially in posterior or chronic uveitis.
  • ANA and anti-CCP — selected cases with joint symptoms.
  • Toxoplasma IgG and IgM — posterior uveitis.
  • FBC, ESR, CRP — baseline inflammatory assessment.
  • Chest X-ray — MBS item 58500 — sarcoidosis (bilateral hilar lymphadenopathy) and TB screening.

GP-orderable pathology items include standard consult items 23/36/44 and rebatable pathology for the investigations above. An ophthalmologist will often direct the workup after examination.

B. Evidence appraisal

What the evidence says about key clinical questions

Should first-attack anterior uveitis be investigated or treated empirically? The evidence supports treating first-attack mild unilateral anterior uveitis empirically in healthy young adults. Extensive workup at first presentation has not been shown to change initial management and may not be cost-effective. The recommendation is to investigate recurrent, atypical, bilateral, or posterior cases, where systemic disease is more likely to be found. RANZCO endorses this approach.

Does adalimumab reduce uveitic flares in non-infectious posterior and intermediate uveitis? The VISUAL I trial (Rosenbaum et al., NEJM 2016) demonstrated that adalimumab (Humira) significantly delayed the time to treatment failure compared with placebo in adults with active non-infectious intermediate, posterior, or panuveitis. Time to treatment failure was significantly longer in the adalimumab group (median not reached vs 13 weeks in placebo, p < 0.001). Based on this evidence, adalimumab is listed on the PBS under Authority Required for non-infectious intermediate, posterior, and panuveitis meeting specific criteria — prescribed by a specialist after failure of conventional immunosuppressants.

Is topical steroid alone sufficient for anterior uveitis? For most acute anterior uveitis, prednisolone acetate 1% eyedrops (started hourly and tapered) combined with a cycloplegic agent such as cyclopentolate (to prevent synechiae and relieve ciliary spasm) is effective first-line treatment, guided by an ophthalmologist. Posterior and refractory disease requires systemic therapy. Abrupt cessation of topical steroids risks rebound inflammation — ophthalmologist-supervised tapering is essential.

C. Treatment framework — ophthalmology-led

The GP role during the waiting period

While arranging same-day ophthalmology review, the GP’s role is limited to:

  • Documenting and recording visual acuity.
  • Providing oral analgesics (paracetamol) for pain.
  • Recommending dark glasses for photophobia.
  • Reassuring the patient and explaining why specialist review is urgent.

Do not prescribe topical steroids or topical cycloplegics in general practice before ophthalmology assessment. Topical steroids can worsen herpetic or fungal keratitis, and ophthalmology needs to assess intraocular pressure before initiating steroid eyedrops.

Treatment by anatomic class (ophthalmologist-directed)

Anterior uveitis:

  • Prednisolone acetate 1% eyedrops — initially hourly, then progressively tapered over 4–6 weeks depending on response. Available on the PBS general schedule.
  • Cyclopentolate 1% TDS or atropine 1% daily — prevents posterior synechiae and reduces ciliary spasm. PBS general schedule.
  • Intraocular pressure must be monitored throughout — steroid-induced ocular hypertension is a common complication.

Intermediate and posterior uveitis / refractory anterior:

  • Oral prednisolone 0.5–1 mg/kg/day, tapered under specialist supervision.
  • Steroid-sparing immunosuppressants — methotrexate, mycophenolate mofetil, azathioprine — for chronic or recurrent disease. PBS Authority Required for autoimmune indications.
  • Adalimumab (Humira) — PBS Authority Required for non-infectious intermediate, posterior, or panuveitis meeting criteria (VISUAL trial evidence). Specialist-initiated only.

Infectious uveitis:

  • Herpetic uveitis (HSV or VZV) — oral valaciclovir 1 g TDS or aciclovir per eTG. Topical antiviral may be added.
  • Toxoplasmic chorioretinitis — pyrimethamine plus sulfadiazine plus folinic acid, or alternative regimens.
  • CMV retinitis (in HIV) — valganciclovir plus antiretroviral therapy.
  • Syphilitic uveitis — IV benzylpenicillin per eTG.
  • TB uveitis — quadruple antitubercular therapy directed by an infectious diseases physician.

Treating the underlying systemic condition

Uveitis associated with ankylosing spondylitis or other spondyloarthropathies benefits from rheumatology review. Anti-TNF therapies (adalimumab, certolizumab) treat both the spinal disease and the uveitis in many patients. IBD-associated uveitis should be managed with a gastroenterologist. Sarcoidosis is managed with respiratory or general medicine input.

D. Special populations

Aboriginal and Torres Strait Islander patients

Higher rates of tuberculosis in some remote communities mean that TB uveitis should be considered earlier in the differential diagnosis. Syphilis also has higher rates in some Indigenous communities and should be excluded in any uveitis presentation. Coordinate with Aboriginal Community Controlled Health Organisations (ACCHOs) and ophthalmology services. Closing the Gap PBS co-payment arrangements apply. Refer for ATSI Health Assessment MBS item 715 as appropriate.

Immunocompromised patients

HIV-positive patients are at risk of CMV retinitis (typically when CD4 count is below 50 cells/µL) and of other opportunistic infections causing posterior uveitis. Any immunocompromised patient presenting with floaters or reduced vision needs urgent ophthalmology — this is not an acute anterior uveitis presentation and warrants a very different workup.

People on immune checkpoint inhibitors (ipilimumab, nivolumab, pembrolizumab) for cancer treatment may develop immune-related uveitis as an adverse effect. This should be reported to the treating oncologist immediately and ophthalmology review arranged.

Children and juveniles (JIA-associated uveitis)

Juvenile idiopathic arthritis (JIA) carries a risk of chronic anterior uveitis that is often asymptomatic — children may develop significant intraocular damage before they notice any problem. This is a trap: children with JIA need regular ophthalmology screening regardless of eye symptoms. The frequency of screening depends on JIA subtype, ANA status, age, and disease duration — ophthalmology determines the schedule.

Long-term steroid complications

Patients on extended topical or systemic steroids for chronic uveitis should be monitored for:

  • Steroid-induced glaucoma — intraocular pressure checks at each ophthalmology visit.
  • Posterior subcapsular cataract — common with chronic topical and systemic steroids.
  • Osteoporosis — calcium, vitamin D, and bisphosphonate consideration for long-term systemic steroid users per standard Australian guidelines.
  • Vaccination review — immunocompromised patients on methotrexate, mycophenolate, or adalimumab should have NIP-funded influenza and pneumococcal vaccines and should avoid live vaccines. See Australian Immunisation Handbook.

When to escalate

Same-day ophthalmology (urgent):

  • Any new presentation of red eye with photophobia, pain, and reduced vision — until uveitis and its mimics are excluded.
  • Known uveitis patient with sudden worsening or new visual change.

Emergency department (category 1 — ambulance if needed):

  • Sudden severe visual loss in a red eye — acute angle-closure glaucoma.
  • Post-surgical eye with severe pain and visual loss — endophthalmitis.
  • Sudden painless vision loss — central retinal artery occlusion.
  • Red eye in a patient with giant cell arteritis symptoms — arteritic ischaemic optic neuropathy.

Specialist referral (1–2 weeks) for:

  • Recurrent uveitis without a systemic diagnosis — rheumatology or ophthalmology.
  • Suspected sarcoidosis, IBD, or MS as underlying cause.
  • Long-term uveitis with complications needing cataracts or glaucoma management.

What this article is and is not

This article provides general patient education about uveitis for people living in Australia. It is not a substitute for professional medical advice and does not replace an ophthalmologist’s assessment and individualised management plan. The clinical details here reflect current Australian guidelines but may not cover every clinical situation. Always consult your GP or ophthalmologist about your specific circumstances. If you have sudden vision loss or severe eye pain, seek emergency care immediately.


Sources cited

Frequently asked questions

  • How is uveitis different from conjunctivitis?

    Conjunctivitis gives a diffuse redness and usually a discharge, with minimal pain and no change in vision. Uveitis causes a 'circumlimbal' ring of redness around the cornea edge, significant light sensitivity, aching pain, and often blurred vision. Pupils may be irregular in uveitis due to inflammation-caused adhesions. If vision is affected or light sensitivity is marked, uveitis is the diagnosis until an ophthalmologist says otherwise.

  • What is HLA-B27 and why does it matter in uveitis?

    HLA-B27 is a protein found on immune cells in about 8% of white Australians. People who carry it have a strongly increased risk of acute anterior uveitis — roughly 32% of cases are HLA-B27 related. HLA-B27 is also linked to ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and inflammatory bowel disease. A person presenting with acute anterior uveitis who has back pain, joint symptoms, or bowel symptoms warrants testing for HLA-B27 and rheumatology review.

  • Why can't GPs just prescribe steroid eyedrops without ophthalmology review?

    Using topical steroids without ophthalmology input carries real risks. Steroid eyedrops raise intraocular pressure and can cause steroid-induced glaucoma — which is irreversible if missed. Secondly, they can worsen infectious causes of red eye, including herpetic or fungal keratitis. An ophthalmologist performs slit-lamp examination to grade the inflammation, rule out dangerous mimics, monitor intraocular pressure, and decide the appropriate steroid potency and tapering speed.

  • When does uveitis become a medical emergency?

    Call an ambulance or go to an emergency department if a painful red eye is accompanied by sudden severe vision loss, halos around lights, or a rock-hard eye with a fixed mid-dilated pupil — this suggests acute angle-closure glaucoma, which can cause permanent blindness within hours. Also go to ED if there has been recent eye surgery and the eye is inflamed — that is endophthalmitis until proven otherwise, another surgical emergency. Same-day ophthalmology (not just GP) is needed for any new uveitis presentation.

  • Can uveitis come back after treatment?

    Yes. Anterior uveitis associated with HLA-B27 is classically recurrent — patients may have multiple episodes over years, each requiring a fresh steroid taper supervised by an ophthalmologist. Posterior or intermediate uveitis linked to systemic diseases like sarcoidosis or inflammatory bowel disease can become chronic and require long-term immunosuppression. The ophthalmologist tracks the pattern and guides whether maintenance treatment or biologic therapy (such as adalimumab) is appropriate.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.