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Anterior uveitis

Recognise inflammation of the iris and anterior uveal tract, arrange prompt ophthalmic confirmation, and understand supervised treatment, targeted investigation and surveillance for visual complications.

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Painful photophobic red eye

Anterior uveitis can threaten vision and cannot be confirmed from redness alone; microbial keratitis and other ocular emergencies may look similar.

Action: Arrange urgent ophthalmic assessment, usually within 24 hours, and use same-day emergency assessment for marked visual loss, severe pain, a hypopyon or diagnostic concern for infection. Do not start an ocular steroid before the eye has been appropriately examined.

Open the sections you need. The overview is shown first.
01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The uvea comprises the iris, ciliary body and choroid. In anterior uveitis, the clinically apparent inflammation is predominantly in the anterior chamber and adjacent anterior structures. Many acute cases present with unilateral aching pain, light sensitivity and blurred vision, but chronic disease can be less symptomatic. Ask when symptoms began, whether this resembles a previous confirmed episode, and whether there are floaters, flashes or a wider visual disturbance that might suggest additional posterior involvement. A previous label of uveitis should help the history without replacing examination.

The key diagnostic examination is slit-lamp assessment. Cells within the anterior chamber indicate inflammatory cellular activity, while flare reflects protein leakage. Record baseline visual acuity, pupil shape, corneal findings and intraocular pressure where safe and within competence. Pressure can be low or raised, so a single pressure result neither establishes nor excludes uveitis. A hypopyon is an important finding requiring urgent assessment of cause; infection, severe inflammatory disease and recent ocular intervention change the differential. Examine beyond the anterior segment when the history or specialist findings indicate it.

Treatment suppresses damaging inflammation, relieves ciliary spasm and reduces the risk of adhesions between the iris and lens. The balance depends on aetiology: immune-mediated disease and infection-associated inflammation may need different combinations of therapy. Ophthalmology therefore sets the steroid preparation, initial intensity, cycloplegic agent, review timing and taper. Explain this plan in clear written terms, including which eye to treat and how the dose changes. Clinical improvement does not justify independent abrupt withdrawal or unsupervised resumption from an old bottle at a future recurrence.

Key points

  • Anterior uveitis involves inflammation at the front of the uveal tract, commonly producing aching pain, photophobia, redness and blurred vision.
  • Slit-lamp evidence of anterior chamber cells and flare supports the diagnosis and allows activity to be monitored.
  • Ciliary injection and a small or irregular pupil are useful clues, but their absence does not exclude inflammation.
  • Both direct and consensual photophobia can occur; a quiet-looking eye does not reliably exclude chronic uveitis.
  • Topical corticosteroid and cycloplegic treatment is selected and adjusted by ophthalmology after infection assessment.
  • Recurrence, chronicity and systemic clues guide investigation; every uncomplicated first episode does not require the same broad blood-test panel.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
01

Idiopathic and immune-mediated disease

Many episodes have no identified cause, while others accompany spondyloarthritis, inflammatory bowel disease, psoriasis or systemic inflammatory conditions. The ocular pattern helps direct assessment.

02

Infection-associated inflammation

Herpetic and other infections can cause or accompany anterior inflammation. Recognising an infectious component changes treatment because corticosteroid exposure may need additional targeted antimicrobial cover.

03

Local ocular triggers

Trauma and previous ocular intervention can be relevant. Pain and deteriorating vision after surgery also require consideration of infection rather than automatic attribution to sterile inflammation.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
  1. 1
    Blood–aqueous barrier disruption

    Inflammation increases passage of cells and protein into aqueous humour. Slit-lamp examination detects these changes as anterior chamber cells and flare, supporting diagnosis and activity assessment.

  2. 2
    Ciliary spasm

    Inflammation around the iris and ciliary body produces pain during pupil movement and focusing. This helps explain light sensitivity and the symptomatic role of prescribed cycloplegia.

  3. 3
    Adhesion formation

    Inflamed iris tissue can adhere to the anterior lens surface, creating posterior synechiae. These adhesions distort pupil shape and may interfere with normal aqueous flow.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Pain and light sensitivity

An aching eye with photophobia, sometimes provoked by light entering the other eye, supports intraocular inflammation but must be interpreted with the rest of the examination.

Anterior chamber inflammation

Cells and flare seen on slit-lamp examination provide evidence of inflammation and help grade activity; these findings cannot be assessed reliably from an external photograph.

Pupil and redness pattern

Perilimbal ciliary injection and a small or irregular pupil are suggestive; posterior synechiae can distort the pupil and complicate dilation.

Associated medical symptoms

Inflammatory back pain, psoriasis, bowel inflammation, oral or genital ulcers and infection exposures help direct a focused systemic assessment when relevant.

Red flags requiring action

  • New visual reduction, severe pain, a hypopyon or rapidly progressive redness requires same-day emergency assessment.
  • Recent intraocular surgery or injection with pain and declining vision raises concern for endophthalmitis rather than an ordinary recurrent episode.
  • A corneal epithelial defect or dendritic lesion requires an infectious corneal assessment before steroid treatment is considered.
05InvestigationsWhat to request, why it matters and how to interpret it.
Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

  1. 01
    Visual acuity and slit-lamp examinationFirst step
    Why
    Confirm anterior inflammation and document its effect on function.
    Interpretation and limitations
    Record cells, flare, keratic precipitates, corneal integrity and pupil findings; an epithelial ulcer or alternative lesion changes the treatment pathway.
  2. 02
    Intraocular pressure measurement
    Why
    Detect pressure disturbance and establish a treatment-monitoring baseline.
    Interpretation and limitations
    Pressure can change because of inflammation, angle mechanisms or steroid response; a normal initial measurement does not remove the need for subsequent monitoring.
  3. 03
    Dilated posterior-segment assessment when indicated
    Why
    Determine whether inflammation or complications extend beyond the anterior chamber.
    Interpretation and limitations
    Floaters, unexplained visual loss or specialist findings may prompt retinal examination and imaging for posterior inflammation or macular oedema.
  4. 04
    Targeted systemic and infection testing
    Why
    Investigate a plausible associated cause and inform safe therapy.
    Interpretation and limitations
    Recurrent, bilateral, chronic or atypical disease may justify directed testing for inflammatory or infectious disorders; results must be interpreted in the clinical context.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
01

Microbial keratitis

Corneal infection can cause a painful photophobic red eye and secondary chamber inflammation. A corneal infiltrate or epithelial defect requires a corneal infection pathway.

02

Acute angle closure

Severe ocular pain, nausea, reduced vision and an abnormal pupil can indicate acute pressure elevation. Corneal haze and pressure assessment help distinguish this emergency.

03

Endophthalmitis

Intraocular infection may cause pain, redness, visual loss and a hypopyon, particularly after surgery or injection. Delay while treating presumed routine uveitis can endanger vision.

07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Suspected episodeObtain prompt ophthalmic confirmationFirst stepPain, photophobia, ciliary redness or visual disturbance raises concern for anterior uveitis.
  1. 1Document acuity and relevant history, including contact lenses, ocular procedures, prior uveitis and any systemic illness.
  2. 2EscalationArrange ophthalmic assessment urgently, generally within 24 hours, with immediate escalation for severe findings or possible infection.
  3. 3Avoid empirical steroid drops while the diagnosis and corneal integrity remain uncertain, and give clear instructions about deteriorating vision.
02Confirmed inflammationFollow the specialist anti-inflammatory and cycloplegic planOphthalmology has established anterior uveitis and assessed relevant infectious alternatives.
  1. 1Start the prescribed steroid preparation at the specified frequency and use the selected cycloplegic when indicated for pain and adhesion prevention.
  2. 2Explain administration, bottle handling, temporary blur and the need to follow a written taper rather than adjusting treatment independently.
  3. 3Review activity and pressure at the interval determined by severity, treatment intensity and complication risk, reducing treatment according to examination findings.
03Recurrent or resistant diseaseReconsider cause and protect long-term visionInflammation recurs, fails to respond as expected or requires prolonged treatment.
  1. 1AlternativeCheck adherence, drop technique and whether an infectious or other alternative diagnosis has been overlooked.
  2. 2Arrange focused systemic assessment and additional ocular imaging or testing through the specialist team when the pattern warrants it.
  3. 3EscalationCoordinate escalation to local or systemic specialist therapy where necessary, with clear responsibility for monitoring and relapse access.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions
Suppresses steroid-responsive anterior inflammation once an appropriate diagnosis and infection assessment have been completed.

Prednisolone acetate 1% eye drops, Pred Forte

The adult SmPC describes one to two drops into the affected eye two to four times daily; during the initial 24 to 48 hours this may be increased to two drops hourly. Ophthalmology individualises intensity, duration and taper to the examined inflammatory activity.

Shake the suspension and use punctal occlusion for one minute. Untreated purulent infection, epithelial herpes simplex, fungal and mycobacterial ocular infection are contraindications. Treatment beyond ten days requires strict ophthalmic supervision with pressure checks; corneal or scleral thinning increases perforation risk.

Produces cycloplegia and mydriasis to relieve ciliary spasm and help prevent iris–lens adhesions.

Cyclopentolate 1% eye drops, Minims

For adult uveitis and posterior synechiae, the SmPC describes one to two drops every six to eight hours, with strength adjusted to clinical response. Ophthalmology determines the treatment period and review.

Exclude allergy and narrow-angle glaucoma or a shallow anterior chamber that predisposes to angle closure. Compress the lacrimal sac for one minute to reduce systemic absorption and assess anticholinergic risks, including cardiac disease and interacting medicines. The SmPC advises avoiding use during pregnancy unless essential and states that this preparation should not be used during breastfeeding; obtain specialist advice if either applies. Do not drive until vision is clear. Discard the single-use unit after administration.

08ComplicationsImportant consequences, why they occur and why they matter clinically.
01

Posterior synechiae and pressure disturbance

Adhesions may distort the pupil and compromise aqueous movement, while inflammation and steroid response can also alter pressure. These mechanisms require examination and continued monitoring.

02

Cataract and macular oedema

Inflammation and treatment exposure can contribute to lens opacity, while macular oedema can impair central vision. Incomplete visual recovery should prompt examination beyond symptom control.

03

Chronic or recurrent visual damage

Repeated inflammatory episodes can accumulate structural injury and treatment burden. Coordinated follow-up, cause-directed assessment and a clear relapse pathway help protect long-term visual function.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.
  • Follow the planned ophthalmic review even when pain improves, because anterior chamber activity and steroid-induced pressure elevation may not produce obvious symptoms.
  • Check visual acuity, inflammatory activity and intraocular pressure, adding posterior assessment or imaging when visual recovery is less than expected.
  • Ensure the patient understands the exact treated eye, preparation strength, dose changes and next review date; resolve conflicting written instructions promptly.
  • Review recurrent symptoms urgently instead of restarting an old steroid bottle before infection or a different red-eye diagnosis has been excluded.
  • Explain that increasing pain, a new corneal opacity, worsening vision or marked treatment-related symptoms requires contact before the scheduled appointment.
10Special situationsVariants, exceptions and circumstances that change the usual approach.

Consensual photophobia supports localisation

Pain in the affected eye when light enters the fellow eye can reflect iris movement and ciliary spasm. It is a useful clue, not a substitute for slit-lamp confirmation.

Pressure has several mechanisms

Inflammation may alter aqueous production or drainage, adhesions can change angle anatomy, and corticosteroids can raise pressure. Monitoring must therefore continue across the treatment course.

Children can present quietly

Some chronic paediatric uveitis is initially asymptomatic, including disease associated with juvenile idiopathic arthritis. Relevant children need their specialist screening schedule rather than symptom-led detection alone.

Investigate a meaningful clinical pattern

Recurrent unilateral episodes with inflammatory back pain and chronic bilateral disease suggest different work-ups. Testing should answer a clinical question rather than follow an identical panel for every patient.

11Common pitfallsFrequent interpretation and management errors.
  1. 01

    Diagnosing uveitis from photophobia alone without examining the cornea and considering infection or other ocular emergencies.

  2. 02

    Treating a hypopyon after recent surgery as a routine inflammatory relapse instead of possible endophthalmitis.

  3. 03

    Stopping or restarting steroid drops without a review plan because pain has improved or familiar symptoms have returned.

  4. 04

    Assuming a normal pressure measurement or little visible redness excludes ongoing disease or the need for follow-up.

Practice

Two practice questions

Question 1 of 20 correct
OphthalmologyOriginal SBA

Evidence of anterior inflammation

A 29-year-old has unilateral aching eye pain, photophobia and blurred vision. The cornea has no epithelial defect. Slit-lamp examination shows anterior chamber cells and flare with a mildly irregular pupil. Which diagnosis best explains these findings?

Sources and review status5 sources · checked 7 Sept 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 7 Sept 2026; clinical approval remains outstanding.

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom