Uveitis (Eye Inflammation)

Uveitis may be caused by infectious agents (bacteria such as Mycobacterium tuberculosis, viruses such as herpes simplex and zoster, parasites such as Toxoplasma gondii, and fungi), autoimmune conditions (ankylosing spondylitis, sarcoidosis, juvenile idiopathic arthritis, lupus), direct ocular trauma, or systemic inflammatory diseases. In approximately 50% of cases despite comprehensive investigation, no specific underlying cause is identified, and these are classified as idiopathic uveitis. The most important diagnostic task is distinguishing infectious from non-infectious uveitis, as treatment strategies differ fundamentally.

Yes, uveitis is a potentially sight-threatening condition that requires prompt medical attention. If left untreated or inadequately managed, intraocular inflammation causes cumulative structural damage — posterior synechiae (iris adhesions), cataract, secondary glaucoma, macular oedema, and retinal or optic nerve damage — any of which can cause significant or permanent vision loss. The severity depends on the anatomical location, the intensity of inflammation, the underlying cause, and how promptly and effectively treatment is initiated. With appropriate management, the majority of uveitis patients retain useful vision.

Yes. Recurrence is common and is one of the defining features of uveitis, particularly in autoimmune forms. HLA-B27-associated anterior uveitis typically follows a pattern of acute self-limiting attacks with recurrence every few months to years. Infectious causes such as herpetic uveitis may recur when antiviral therapy is discontinued. Tuberculous uveitis requires complete antitubercular treatment to prevent relapse. Identifying and treating the underlying systemic cause is therefore the most effective long-term strategy for reducing recurrence frequency and severity.

Yes, if not treated adequately and promptly. Complications of uveitis — including macular oedema, optic nerve damage, retinal detachment, corneal band keratopathy, uveitic glaucoma, and cataract — can all cause permanent vision loss. The risk is higher in posterior uveitis and panuveitis, in chronic and recurrent disease, and when treatment is delayed or compliance is poor. Regular follow-up allows early detection and management of these complications before they cause irreversible structural changes.

Treatment duration depends on the type and cause of uveitis. Acute idiopathic anterior uveitis may resolve within 6–8 weeks with a tapering course of topical steroids, requiring no long-term therapy. Infectious uveitis requires pathogen-specific antimicrobial treatment for defined durations. Chronic autoimmune uveitis — particularly bilateral, posterior, or pan-uveitis — frequently requires sustained systemic immunosuppressive therapy for months to years to maintain inflammation control and prevent organ damage. The goal is always to achieve the minimum effective therapy that controls disease with acceptable side effects.

Early diagnosis is critically important in uveitis. Within the first 24–48 hours of acute anterior uveitis, posterior synechiae (adhesions between the iris and lens capsule) can begin to form; if allowed to become extensive, these cause permanent pupil distortion and increased surgical complexity for any subsequent lens procedures. In posterior uveitis, macular oedema developing undetected over weeks causes photoreceptor loss that may not fully recover even after inflammation is controlled. Prompt specialist review at the onset of symptoms dramatically improves both the speed of inflammation control and the likelihood of preserving full visual function.