Uveitis
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Direct answer
Uveitis is inflammation of the iris, ciliary body or choroid, and the anterior form presents with a painful, photophobic, red eye in which the flush is deepest around the limbus, the pupil is small and irregular, and keratic precipitates clutter the corneal endothelium. Classification is anatomical — anterior, intermediate, posterior or panuveitis — and each pattern carries its own cause list, from HLA-B27-associated ankylosing spondylitis to tuberculosis, sarcoidosis, syphilis and Behçet disease in the Indian clinic. Treatment pairs a cycloplegic such as homatropine or atropine (to break pain and prevent posterior synechiae) with steroids delivered topically, periocularly or systemically, guided by the cause. The two special examinations favourites, Vogt-Koyanagi-Harada disease and sympathetic ophthalmia, are both bilateral granulomatous panuveitides.
What you must remember
- Anterior uveitis triad: ciliary limbal flush, miosis with a sluggish pupil, keratic precipitates; cells and flare in the anterior chamber on slit lamp.
- Granulomatous uveitis shows mutton-fat keratic precipitates, Koeppe and Busacca iris nodules and posterior synechiae; non-granulomatous disease shows fine KPs and aqueous flare.
- HLA-B27 associates with acute recurrent anterior uveitis in ankylosing spondylitis, reactive arthritis and inflammatory bowel disease — young men with a stiff, painful back and a red eye.
- Behçet disease: recurrent hypopyon uveitis with oral and genital ulceration and skin pathology; VKH: bilateral granulomatous panuveitis with meningism, tinnitus, dysacousia, alopecia, poliosis and vitiligo, giving a sunset-glow fundus.
- Sympathetic ophthalmia is bilateral granulomatous panuveitis following penetrating injury or surgery to one eye, usually appearing two weeks to three months later; prevention is enucleation of a hopelessly blind, badly disrupted globe within about 14 days.
- Intermediate uveitis (pars planitis) affects young people with floaters and snowball or snowbank exudates over the pars plana; macular oedema is the threat to vision.
- Toxoplasma retinochoroiditis produces a fluffy white retinitis next to an old pigmented scar — the "headlight in the fog" — treated with antiparasitics plus steroids (steroids never alone).
- Never start steroids without cycloplegia and, where possible, a work-up: chest radiograph, Mantoux, syphilis serology, HLA-B27 and sarcoid markers are the Indian standard panel.
A unilateral red eye in a young man, worked through
A 27-year-old presents with right eye pain, photophobia and blurred vision for three days; he mentions early-morning low-back stiffness that responds to exercise. Vision is 6/18; the eye shows deep limbal injection, a small irregular pupil and fine keratic precipitates, with two-plus cells and flare in the anterior chamber. The pattern is acute non-granulomatous anterior uveitis, and the back story flags ankylosing spondylitis: order HLA-B27, inflammatory markers and a sacroiliac radiograph, but do not wait for results to treat. Start homatropine 2 per cent twice daily to immobilise the ciliary body and prevent posterior synechiae, and prednisolone acetate 1 per cent hourly, tapered over weeks against the cell count. Review at 48 hours: falling cells and a dilated round pupil mean response; a fibrin-filled pupil or rising pressure means escalation to oral steroids and a glaucoma review. Had the KPs been mutton-fat with iris nodules, the pathway would widen to granulomatous causes — tuberculosis, sarcoidosis, VKH — before any steroid plan. Had the patient returned after eye surgery with a quiet partner eye turning granulomatous, sympathetic ophthalmia would top the list. The discipline is the same each time: characterise the inflammation, treat early with cycloplegia plus steroids, and chase the cause in parallel.
Where candidates slip
Three marks are lost predictably. One: treating uveitis with antibiotics — most cases are non-infective or immunological, and the emergency is suppression of inflammation, not antimicrobial cover. Two: forgetting the fellow eye and the systemic cause; an examiner who asks about oral ulcers, vitiligo or back pain is handing the diagnosis over. Three: the sympathetic ophthalmia timeline — any granulomatous inflammation in the fellow eye weeks to months after penetrating trauma or surgery is sympathetic ophthalmia until proven otherwise, and steroids or immunosuppression must start immediately; the enucleation-of-the-injured-eye rule applies only within the first two weeks of a devastating injury.
Frequently asked questions
What distinguishes granulomatous from non-granulomatous uveitis?
Mutton-fat keratic precipitates, iris nodules (Koeppe and Busacca) and dense posterior synechiae in granulomatous disease, versus fine KPs and aqueous flare in non-granulomatous inflammation.
Which conditions link HLA-B27 with anterior uveitis?
Ankylosing spondylitis, reactive arthritis, inflammatory bowel disease and psoriatic arthritis — typically acute, recurrent, unilateral anterior uveitis in young men.
What is sympathetic ophthalmia and how is it prevented?
Bilateral granulomatous panuveitis following penetrating injury or surgery to the other eye, mostly within two weeks to three months; prevented by enucleating a hopelessly injured eye within about 14 days.
Why are cycloplegics mandatory in anterior uveitis?
They relieve ciliary spasm and pain and keep the pupil moving, preventing posterior synechiae, secondary angle closure and a fixed small pupil.
What are the systemic features of VKH syndrome?
Meningism, tinnitus and dysacousia, alopecia, poliosis and vitiligo accompanying bilateral granulomatous panuveitis with a sunset-glow fundus.
How does toxoplasma retinochoroiditis appear?
A fluffy white focal retinitis adjacent to an old pigmented scar, the headlight in the fog, treated with antiparasitic drugs covered by steroids.