Q3 LONG ANSWER 10M ★ High-yield

Describe the complications of uveitis and the principles of its management.

Ophthalmology · 3rd Professional

Complications of Uveitis

The complications, rather than the inflammation itself, are what blind the patient — and most are preventable by adequate early treatment

Complication	Mechanism and management
Cystoid macular oedema	The commonest cause of visual loss in uveitis. Breakdown of the blood-retinal barrier with fluid accumulation in the outer plexiform layer, giving a petaloid pattern on angiography and cystic spaces on OCT. Treated by controlling the inflammation, with periocular or intravitreal steroid, acetazolamide and immunosuppression
Complicated cataract	Characteristically posterior subcapsular, from both the inflammation and the steroids. Surgery is deferred until the eye has been quiet for at least 3 months, with perioperative steroid cover; the results are otherwise poor
Secondary glaucoma	By several mechanisms, which have to be told apart because the treatment differs: trabeculitis and clogging of the meshwork by cells and fibrin (open angle, treat the inflammation); steroid response; peripheral anterior synechiae (chronic angle closure); and seclusio pupillae with iris bombe (pupil block), which requires an urgent laser iridotomy
Band keratopathy	Calcium in Bowman membrane in the interpalpebral band; classical in chronic uveitis of juvenile idiopathic arthritis. Treated by EDTA chelation
Hypotony and phthisis bulbi	Ciliary body shutdown or a cyclitic membrane pulling on the ciliary body; leads to a soft, shrunken, blind eye. Largely irreversible, and the end point of neglected uveitis
Posterior segment	Epiretinal membrane; choroidal neovascularisation; tractional or exudative retinal detachment; optic atrophy; and persistent vitreous opacities

Cystoid Macular Oedema — the Principal Cause of Visual Loss

Cystoid macular oedema (CMO) is the accumulation of fluid in cystic spaces of the outer plexiform (HENLE) layer of the macula, following breakdown of the blood-retinal barrier. It is the commonest cause of visual loss in uveitis of every anatomical class

The Ladder of Treatment

Step 0 — exclude and treat infection first.
Immunosuppressing a patient with tuberculous, syphilitic, herpetic or toxoplasmic uveitis is catastrophic, and this step comes before every other → step 1 — topical: prednisolone acetate 1% intensively with a cycloplegic.
Sufficient for most anterior uveitis; ineffective for posterior disease, because drops do not reach the back of the eye → step 2 — periocular: posterior sub-Tenon or orbital floor triamcinolone, for unilateral posterior or intermediate disease and for macular oedema → step 3 — intravitreal: triamcinolone, or a sustained-release dexamethasone or fluocinolone implant.

Mechanism	Findings	Treatment
Trabeculitis and cellular clogging	Open angle; active inflammation with heavy cells and fibrin	Treat the inflammation more intensively; aqueous suppressants
Steroid response	Open angle; the eye is quiet but the pressure is rising on treatment; after 2 to 6 weeks of steroid	Reduce the steroid potency or change to a weaker agent (loteprednol, fluorometholone); add aqueous suppressants
Seclusio pupillae with iris bombe	360-degree posterior synechiae; the peripheral iris bowed forward; a shallow peripheral anterior chamber with a normal central depth	Urgent laser iridotomy — an emergency
Peripheral anterior synechiae	Closed angle on gonioscopy; chronic disease	Aqueous suppressants; surgery if uncontrolled
Neovascular glaucoma	New vessels on the iris and in the angle, after ischaemic posterior segment disease	Anti-VEGF, panretinal photocoagulation, drainage surgery
POSNER-schlossman syndrome	Very high pressure with minimal inflammation and an open angle; recurrent and unilateral	Topical steroid and aqueous suppressants; self-limiting attacks
Hypotony (the converse)	Ciliary body shutdown or a cyclitic membrane	Treat the inflammation aggressively; it heralds phthisis

Monitoring and Applied Aspects

Monitor at every visit — visual acuity; anterior chamber cells (not flare) to titrate treatment; intraocular pressure, which both the disease and the treatment raise; the lens; and the macula by OCT
Systemic monitoring on immunosuppression — full blood count, liver and renal function; blood pressure and glucose on steroid; bone protection with calcium, vitamin D and a bisphosphonate where appropriate; and screening for tuberculosis and hepatitis before biological agents
Exclude infection before immunosuppressing; this is the single most important rule in uveitis management, and in India it means thinking about tuberculosis in every case

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