Uveitis: Classification, Clinical Features, Investigations and Emergency Management

Scope. Uveitis is inflammation of the uveal tract—the iris, ciliary body and choroid—but inflammation may also involve the retina, vitreous, optic nerve and sclera. It is a sight-threatening diagnosis that can arise from infection, autoimmune disease, trauma, malignancy or an apparently idiopathic process. This resource expands the supplied uveitis slides into a detailed guide for emergency medicine students, including triage, anatomy, patterns of inflammation, targeted investigations, treatment principles, complications and follow-up.

Learning objectives

• Define uveitis and relate symptoms to the anatomic part of the eye involved.
• Classify uveitis anatomically, clinically, by time course and by cause.
• Recognise anterior, intermediate, posterior and panuveitis patterns and their complications.
• Distinguish uveitis from conjunctivitis, keratitis, scleritis and acute glaucoma.
• Perform a safe emergency assessment and select focused laboratory and imaging tests.
• Explain specialist-directed treatment, including corticosteroids, cycloplegics, antimicrobials, immunomodulators and complication control.

1. Anatomy and physiology of the uvea

The blood–ocular barrier normally limits movement of proteins and immune cells into the aqueous and vitreous. Inflammation disrupts this barrier, producing cells (white blood cells) and flare (protein) in the anterior chamber, vitreous haze, vascular leakage and tissue damage.

Neighbouring eye structures in the supplied anatomy slides

2. Classification

2.1 Anatomical classification

• Anterior uveitis: inflammation mainly in the iris (iritis) and/or ciliary body (iridocyclitis).
• Intermediate uveitis: inflammation centred in the vitreous, pars plana and peripheral retina; pars planitis is a subset when no infection or systemic disease is identified.
• Posterior uveitis: choroiditis, retinitis, neuroretinitis or retinal vasculitis.
• Panuveitis: clinically important inflammation in anterior chamber, vitreous and posterior segment.

2.2 Time course and pattern

3. Causes

3.1 Infectious causes

• Viral: herpes simplex, varicella-zoster, cytomegalovirus and HIV-associated infections; Zika and other arboviral causes are considered only when exposure and local epidemiology fit.
• Bacterial: syphilis, tuberculosis, brucellosis and leptospirosis; Lyme disease where epidemiologically relevant; and postoperative or endogenous bacterial infection.
• Parasitic: ocular toxoplasmosis, toxocariasis and other region-specific infections.
• Fungal: Candida or Aspergillus endogenous endophthalmitis, especially after intravenous drug use, prolonged hospitalisation, surgery or immunosuppression.

3.2 Non-infectious inflammatory and immune causes

• HLA-B27-associated ankylosing spondylitis, reactive arthritis, psoriatic arthritis and inflammatory bowel disease.
• Other reported associations include Kawasaki disease, multiple sclerosis and Whipple disease; age, systemic features and ocular pattern determine how relevant each is.
• Juvenile idiopathic arthritis (often quiet chronic anterior uveitis in children).
• Sarcoidosis, Behçet disease, systemic lupus, granulomatosis with polyangiitis and relapsing polychondritis.
• Vogt–Koyanagi–Harada disease, sympathetic ophthalmia and birdshot chorioretinopathy in appropriate populations.
• Tubulointerstitial nephritis and uveitis (TINU), idiopathic intermediate uveitis and drug-induced inflammation.

3.3 Traumatic, postoperative and masquerade causes

Blunt or penetrating trauma, intraocular surgery, retained lens material and chemical injury can trigger inflammation. Masquerade syndromes such as intraocular lymphoma, retinoblastoma in a child, leukaemic infiltration or metastatic disease can mimic uveitis. Atypical, unilateral, steroid-resistant, recurrent or progressively worsening “uveitis” requires re-evaluation rather than endless escalation of steroids.

4. Clinical features by anatomic site

4.1 Anterior uveitis

• Deep aching eye pain, often worse in bright light.
• True photophobia: light shone in the normal eye causes pain in the affected eye because the inflamed iris and ciliary muscle contract.
• Blurred vision, watering and a red ring around the cornea (ciliary flush).
• Small, irregular or poorly reactive pupil; posterior synechiae may produce an irregular shape.
• Slit-lamp cells and flare, keratic precipitates, fibrin, hypopyon or iris nodules.
• Intraocular pressure may be low early, normal or high when trabecular inflammation, steroid response or herpetic trabeculitis is present.

4.2 Intermediate uveitis

Floaters, blurred vision and reduced contrast are common, with less pain and redness than anterior uveitis. Vitreous cells/haze, snowballs and snowbanking at the pars plana, retinal vasculitis and macular oedema may occur. Bilateral disease is common. Consider sarcoidosis, multiple sclerosis, infections and paediatric inflammatory disease before labelling it idiopathic.

4.3 Posterior uveitis

Posterior disease usually causes painless visual symptoms: floaters, flashes, scotomas, reduced central vision, metamorphopsia or colour change. Fundus findings may include chorioretinal lesions, retinitis, vasculitis, optic-disc swelling, haemorrhage or macular oedema. Pain and external redness are not reliable exclusion criteria.

4.4 Panuveitis

Panuveitis combines anterior cells/flare with vitreous haze and posterior lesions. Severe infection, tuberculosis, syphilis, toxoplasmosis, endogenous endophthalmitis, Behçet disease and sarcoidosis should be considered. It needs urgent specialist assessment and often coordinated systemic evaluation.

5. Red flags requiring emergency referral

6. Examination

1. Assess general condition, fever, rash, arthritis, oral/genital ulcers, lymph nodes, neurological symptoms and immunosuppression.
2. Measure visual acuity in each eye separately, with correction and pinhole if available.
3. Assess pupils, colour vision, fields and relative afferent pupillary defect.
4. Inspect the pattern of redness: ciliary flush suggests anterior uveal/corneal disease rather than conjunctivitis.
5. Use a slit lamp to identify cells, flare, keratic precipitates, fibrin, hypopyon, posterior synechiae, iris nodules and lens changes.
6. Use fluorescein to exclude corneal epithelial disease before topical steroid therapy.
7. Measure intraocular pressure after excluding open globe; high pressure may indicate glaucoma, herpetic uveitis or steroid response.
8. Perform dilated fundus examination for vitreous haze, snowballs, retinitis, choroiditis, vasculitis, disc oedema and macular oedema.
9. Use OCT for macular oedema and optic-disc assessment, fundus photography for baseline documentation, and B-scan when the view is obscured.

7. Differential diagnosis

8. Investigations

Do not order a broad “uveitis panel” indiscriminately. Testing should be guided by phenotype, recurrence, severity, age, exposure and systemic findings.

• Baseline: full blood count, ESR/CRP, renal and liver profile, urinalysis and blood pressure when systemic inflammation or treatment toxicity is possible.
• Infection: syphilis serology for unexplained or posterior disease; HIV testing with consent; TB assessment (symptoms, exposure, chest imaging and microbiology/immune testing as locally appropriate); toxoplasma testing when fundus lesions fit; targeted herpes/CMV testing in atypical hypertensive or unilateral disease.
• Inflammatory disease: HLA-B27 for recurrent acute anterior attacks with compatible symptoms; ANA and paediatric rheumatology assessment for suspected JIA; ACE/chest imaging for sarcoidosis only when clinically indicated; ANCA when vasculitis is suspected.
• Ocular imaging: OCT, fundus photography, fluorescein angiography, optical coherence tomography angiography and B-scan according to the segment involved.
• Sampling: aqueous or vitreous tap/PCR and culture may be required for suspected endophthalmitis, infectious posterior uveitis or steroid-resistant atypical disease.

9. Treatment principles

9.1 Anterior uveitis

• Anti-inflammatory: an ophthalmologist may use topical prednisolone acetate 1% frequently (in severe disease it may be prescribed as often as hourly while awake), then taper slowly according to cells and flare—not simply symptoms. Frequent review is essential.
• Cycloplegia/mydriasis: homatropine, cyclopentolate or atropine may relieve ciliary spasm and prevent posterior synechiae. Example strengths and frequency vary with severity and age; follow the local ophthalmic protocol.
• Infection-specific therapy: herpes-associated disease requires antiviral treatment; syphilis, TB, toxoplasmosis and other infections require appropriate systemic therapy. Corticosteroids are added only with adequate antimicrobial coverage when indicated.
• Complications: treat raised pressure, macular oedema, cataract and synechiae under specialist supervision. Never use miotics in active anterior uveitis without an ophthalmologist’s direction.

9.2 Intermediate, posterior and panuveitis

• Periocular or intravitreal corticosteroid, oral systemic corticosteroid, or (for selected severe sight-threatening inflammation) specialist-directed intravenous methylprednisolone may be required according to the cause and severity.
• For chronic or recurrent non-infectious disease, a uveitis specialist may use steroid-sparing medicines such as methotrexate, azathioprine, mycophenolate mofetil, ciclosporin or tacrolimus; biologic therapy is reserved for selected cases. These treatments need diagnosis-specific laboratory and infection monitoring.
• Anti-infective treatment is essential for infectious retinitis, endophthalmitis or opportunistic disease; immunosuppression alone is dangerous.
• Macular oedema may need local steroid, anti-VEGF or systemic therapy; treatment is guided by OCT and the underlying diagnosis.
• Severe vitreous opacity, retinal detachment, diagnostic uncertainty or non-response may require vitrectomy, biopsy or retinal surgery.

9.3 Systemic and supportive care

• Coordinate treatment of rheumatoid disease, spondyloarthritis, IBD, sarcoidosis, TB, HIV and other systemic causes.
• Monitor blood pressure, glucose, appetite/weight, fluid retention, gastrointestinal symptoms, infection risk, bone health, renal/liver function and blood counts when systemic corticosteroids or immunosuppressants are used; prolonged steroid exposure also increases cataract and glaucoma risk.
• Use protective eyewear, avoid driving while vision is impaired and teach drop technique, spacing and adherence.
• Follow up until the eye is quiet and continue surveillance for recurrence and treatment complications.

10. Immune pathophysiology: how inflammation develops

Uveitis can begin when infection, trauma, tissue injury or immune dysregulation activates inflammatory cells within the eye. The eye normally limits damaging inflammation through the blood–aqueous and blood–retinal barriers and local regulatory signals, including transforming growth factor beta (TGF-β) and interleukin-10 (IL-10). These mechanisms help protect delicate retinal and uveal tissue while preserving useful immune responses.

In non-infectious disease, genetically susceptible patients may develop an immune response against ocular antigens. HLA-B27 is an important association in some recurrent acute anterior uveitis patterns, and variants such as PTPN22 have also been studied; these are susceptibility markers, not diagnostic tests for an individual episode. Activated T-cell pathways, including Th1/Th17 responses, can amplify inflammation and disrupt the ocular barriers. Once the barrier is disrupted, inflammatory cells and proteins enter the aqueous or vitreous, producing cells, flare and tissue injury. In infectious uveitis, the organism itself and the host response both contribute to damage. This explains why immune suppression may help non-infectious disease but can worsen an untreated infection.

11. Medication and post-vaccination associations

The supplied slides list rifabutin, moxifloxacin and reports after vaccination as possible associations. Treat these as medication-safety prompts rather than proof that a drug or vaccine caused an individual episode. Rifabutin-associated uveitis is a recognised uncommon adverse effect, particularly reported with higher exposure and interacting medicines such as macrolides or azole antifungals. The moxifloxacin association and post-vaccination reports are much less useful as stand-alone causal claims; timing, alternative causes and the patient’s full clinical picture must be reviewed.

12. Natural products and the curcumin evidence

The source deck discusses turmeric and a curcumin–phosphatidylcholine preparation (Meriva/Norflo), including a 2010 report of 106 people followed for 12 months and improvement in reported eye discomfort in more than 80%. That report evaluated curcumin as an addition to usual treatment and was not a placebo-controlled trial. It is an interesting research signal, but it does not establish curcumin as a proven treatment, show that it prevents sight loss, or support replacing ophthalmic treatment with turmeric or supplements.

A separate older study and the supplied slides quote oral curcumin 375 mg three times daily; the 2010 phospholipid-complex study used a different preparation. These historical research regimens are not interchangeable and should not be presented as a current standard prescription. The slides also list Uvical and 500 mg curcumin-phytosome/turmeric products and warn about diabetes, gallbladder disease, gastrointestinal upset, pregnancy and breastfeeding. These are slide-level safety prompts, not a complete, current prescribing standard; a clinician or pharmacist should review pregnancy, comorbidities and interactions before any supplement is considered.

For teaching, distinguish a biological rationale or small uncontrolled study from evidence of clinical effectiveness. Commercial preparations vary in formulation and dose and may interact with medicines or cause adverse effects. Patients should discuss supplements with their treating clinician, especially if they take anticoagulants, antiplatelet medicines or multiple long-term medicines. Suspected uveitis remains an urgent eye-care problem: supplements must never delay slit-lamp assessment, prescribed anti-inflammatory treatment or indicated antimicrobial therapy.

13. Epidemiology and prognosis

The supplied slides quote an approximate frequency of 1 in 4,500 people and describe many cases in adults aged about 20–60 years, with men and women affected similarly. They also cite regional differences in anterior uveitis and estimate that uveitis accounts for 10–20% of blindness in the United States. These are broad, older teaching estimates, not Uganda-specific population rates. Published population estimates vary substantially with geography, age structure, case definition and access to ophthalmic diagnosis; patterns also differ by infectious exposures and the underlying cause. Do not apply a figure from a different country as a local prevalence estimate.

Prognosis is often good when the cause is identified and inflammation is controlled promptly, but it depends on the anatomic site, severity, recurrence, associated disease, treatment response and complications. Repeated or chronic inflammation can cause posterior synechiae, cataract, raised intraocular pressure and glaucoma, cystoid macular oedema, hypotony, retinal damage and permanent visual loss. Symptoms can settle before inflammation is fully controlled, so follow-up examination—not pain relief alone—guides treatment tapering. Delayed presentation, posterior involvement, infection, immunosuppression, a single functioning eye or poor follow-up increases the risk of a poor outcome.

14. Complications

15. Nursing and emergency-care actions

• Document pain, acuity, photophobia, pupil shape, pressure (when safe), redness pattern and medication timing.
• Check that drops are administered to the correct eye, at the correct interval, without touching the bottle tip.
• Warn about temporary blurred vision after cycloplegics and the need for sunglasses in bright light.
• Screen for systemic symptoms and treatment toxicity, especially infection and steroid-related hyperglycaemia or hypertension.
• Reinforce that symptom relief does not prove inflammation has resolved; follow-up slit-lamp findings determine tapering.
• Escalate immediately for worse vision, severe pain, new floaters/flashes, vomiting, hypopyon, fever, confusion or inability to administer treatment.

16. Applied cases

Case 1: Recurrent painful red eye

A 30-year-old has sudden unilateral pain, true photophobia, ciliary flush and a small irregular pupil. Slit lamp shows anterior cells and flare. This is acute anterior uveitis. Check for spondyloarthritis, psoriasis, bowel symptoms and infection, refer the same day and begin specialist-directed cycloplegic and anti-inflammatory treatment.

Case 2: Floaters with reduced vision

A patient reports weeks of floaters and blurred vision with minimal redness. Examination shows vitreous haze and macular oedema. Intermediate or posterior uveitis is likely. Arrange OCT, dilated retinal assessment and targeted systemic/infectious work-up; topical conjunctivitis treatment is inadequate.

Case 3: HIV with a white retinal lesion

An immunocompromised patient has reduced vision and a necrotising retinal lesion with vitritis. CMV retinitis, toxoplasmosis, acute retinal necrosis and endogenous infection are important possibilities. This requires urgent ophthalmology/infectious-disease management, targeted anti-infective therapy and careful decisions about corticosteroids.

Case 4: “Uveitis” not responding to steroids

An older adult has unilateral chronic inflammation that worsens whenever steroids are reduced. Consider masquerade syndromes, intraocular lymphoma, retained lens material and infection. Re-examine the diagnosis and obtain specialist imaging or aqueous/vitreous sampling rather than repeatedly increasing immunosuppression.

17. Self-test

1. What structures make up the uveal tract?
2. What is the difference between anterior, intermediate, posterior and panuveitis?
3. What is true photophobia and why does it occur?
4. Name four emergency red flags in a patient with suspected uveitis.
5. Why should corneal ulcer be excluded before steroid drops?
6. Name three infectious causes that are important in Uganda or in immunocompromised patients.
7. What are cells and flare?
8. List four complications of chronic or recurrent uveitis.

Answers

1. Iris, ciliary body and choroid.
2. Anterior affects iris/ciliary body; intermediate centres on vitreous/pars plana; posterior affects choroid/retina/optic nerve; panuveitis involves more than one segment, including anterior, vitreous and posterior disease.
3. Light entering the normal eye causes pain in the affected eye because it triggers contraction of the inflamed iris and ciliary muscle.
4. Reduced vision, severe pain/photophobia, hypopyon, abnormal pupil, corneal ulcer, new floaters/flashes, retinal lesion, proptosis, immunosuppression, recent surgery and systemic toxicity are examples.
5. Steroids can worsen herpes, bacterial and fungal infection, allowing rapid corneal melt or intraocular spread.
6. Examples include tuberculosis, syphilis, toxoplasmosis, herpes viruses, CMV and endogenous fungal infection.
7. Cells are inflammatory leukocytes in the aqueous; flare is protein leakage caused by breakdown of the blood–aqueous barrier.
8. Synechiae, glaucoma, cataract, cystoid macular oedema, hypotony, retinal detachment, optic-nerve damage and permanent visual loss.

Key takeaways

• True photophobia, ciliary flush, miosis/irregular pupil and anterior chamber cells point toward anterior uveitis.
• Floaters, scotomas and reduced vision may indicate posterior inflammation even without a red eye.
• Infection must be actively considered before corticosteroids or immunosuppression.
• Uveitis is a diagnosis requiring eye examination; a symptom-based “pink-eye” prescription is unsafe.
• Control inflammation early and monitor pressure, cataract, synechiae and macular oedema to preserve vision.

References and further reading

• Supplied teaching slides: Uveitis.
• Merck Manual Professional: Overview of Uveitis.
• National Eye Institute: Uveitis.
• EyeWiki: Treatment of Uveitis.
• Uganda Clinical Guidelines: Uveitis section.
• Uganda Ministry of Health: Guidelines for Eye Care.
• Clinical Ophthalmology: adjunctive curcumin study in recurrent anterior uveitis (2010).
• Phytotherapy Research: early curcumin study in chronic anterior uveitis.
• Systematic review: variation in uveitis incidence and prevalence estimates.
• CDC report: uveitis associated with rifabutin therapy.