Page 6 of 18
OP6.2 | Iridocyclitis: Complications, Investigations and Treatment — SDL Guide (Part 3)
Management of Complications: Glaucoma, Cataract, CMO
When complications have developed despite anti-inflammatory treatment, targeted management is required. These decisions require careful balancing of the surgical or pharmacological risk against the risk of ongoing inflammation. The general principle is that suppressing the underlying inflammation is always the first priority — many secondary complications (trabecular glaucoma, early cystoid macular oedema) will partially or fully resolve once the primary inflammatory drive is adequately controlled. Acting on the complication in isolation without addressing the root cause merely treats the effect while the cause continues to do damage. Equally, delaying intervention for iris bombé while waiting for inflammation to settle is dangerous — that complication demands immediate mechanical correction (laser peripheral iridotomy) because every hour of sustained pupillary block worsens angle closure and risks permanent optic nerve damage. Distinguishing which complications require immediate procedural intervention from those that resolve with enhanced anti-inflammatory therapy is the central clinical judgement this section equips you to make.
Secondary glaucoma in uveitis:
Management depends on the mechanism:
- Trabecular/inflammatory glaucoma (open angle): Control inflammation first (IOP often normalises as inflammation settles). If IOP remains elevated, add IOP-lowering drops. Preferred agents: beta-blockers (timolol) or carbonic anhydrase inhibitors (dorzolamide, acetazolamide systemic). Prostaglandin analogues (e.g. latanoprost) should be AVOIDED in active uveitis — they enhance prostaglandin-mediated inflammation and can worsen the uveitis.
- Iris bombé/angle-closure (from seclusio pupillae): Requires laser peripheral iridotomy (LPI) to restore aqueous flow from posterior to anterior chamber, relieving iris bombé. This is the procedure of choice; the iridotomy bypasses the occluded pupil.
- Steroid-induced glaucoma: Switch to a weak-penetration steroid (fluorometholone, loteprednol) or reduce steroid frequency; add IOP-lowering drops. If uncontrolled, surgical filtration (trabeculectomy or drainage tube) may be needed.
Complicated cataract in uveitis:
Cataract surgery in uveitis patients carries higher risk than in the general population — the eye is prone to post-operative uveitis flares, fibrinous reaction, and synechiae. Timing is critical: operate during a quiescent period (uveitis in remission for at least 3 months). Intensive perioperative topical steroids (prednisolone acetate hourly from 3 days before surgery) and NSAIDs (ketorolac) are used. Phacoemulsification with implantation of a rigid (PMMA) or foldable IOL is the technique of choice; posterior chamber IOLs are preferred. Fuchs heterochromic iridocyclitis is a special case — cataract surgery is safe even in the presence of active inflammation and carries a good prognosis.
Cystoid macular oedema (CMO):
First-line: periocular corticosteroids (sub-Tenon's triamcinolone). Second-line: intravitreal triamcinolone or intravitreal dexamethasone implant (Ozurdex) for sustained release. In non-infectious uveitis, anti-VEGF agents (bevacizumab, ranibizumab) have shown benefit in refractory CMO. For CMO complicating intermediate uveitis, vitrectomy can reduce the inflammatory load and resolve oedema in refractory cases.
CLINICAL PEARL
Two steroid-induced complications to monitor at EVERY visit: (1) IOP rise — check IOP at every consultation when a patient is on topical steroids; steroid responders can silently develop glaucoma within weeks. (2) Posterior subcapsular cataract — any reduction in visual acuity in a uveitis patient on steroids must prompt lens examination. In uveitis-related secondary glaucoma, remember the rule: prostaglandin analogues are CONTRAINDICATED (they worsen uveal inflammation). The preferred IOP-lowering agents are beta-blockers and carbonic anhydrase inhibitors. For iris bombé, laser peripheral iridotomy is both diagnostic confirmation and curative treatment — it immediately restores the pressure gradient and collapses the bombé.
SELF-CHECK
A patient with chronic uveitis on long-term topical prednisolone acetate 1% has developed an IOP of 32 mmHg. Which IOP-lowering agent should be AVOIDED in this patient?
A. Timolol 0.5% eye drops
B. Dorzolamide 2% eye drops
C. Latanoprost 0.005% eye drops
D. Systemic acetazolamide
Reveal Answer
Answer: C. Latanoprost 0.005% eye drops
Prostaglandin analogues (latanoprost and the class) are contraindicated in active uveitis because they enhance prostaglandin-mediated inflammation and can precipitate or worsen uveitic flares. In uveitis-related secondary glaucoma, preferred IOP-lowering agents are beta-blockers (timolol), carbonic anhydrase inhibitors (dorzolamide, systemic acetazolamide), and alpha-2 agonists (brimonidine) — all of which are safe in the context of active intraocular inflammation.
Self-Assessment: Complications and Treatment Decisions
Having worked through the complications and treatment of iridocyclitis, test your understanding with the following clinical scenarios. For each question, consider not just the answer but the clinical reasoning: what mechanism underlies the complication? Which step of the therapeutic ladder is indicated? What monitoring is required to prevent treatment-induced complications? The ability to reason through a complication mechanistically — not simply recall a management step — is what distinguishes a clinician who will handle a novel presentation safely from one who is reliant purely on memorised lists. Use each scenario to practise articulating the pathophysiological chain before selecting an answer.
Key themes to consolidate: (1) the mechanistic sequence from posterior synechiae to iris bombé to secondary angle-closure; (2) the role of OCT in detecting silent CMO; (3) why prostaglandin analogues are avoided in uveitis; (4) the timing principle for cataract surgery in uveitis (quiescence first); and (5) why JIA-associated uveitis is screened even when asymptomatic.