A 58-year-old man presents to the ophthalmology clinic with progressive vision loss over 3 months. He has a history of chronic uveitis secondary to ankylosing spondylitis, treated with topical corticosteroids for the past 2 years. On examination, intraocular pressure (IOP) is 38 mmHg in both eyes. Gonioscopy shows an open angle with normal-appearing trabecular meshwork. Anterior chamber shows 2+ inflammatory cells and flare. What is the most likely mechanism of glaucoma in this patient?

Explanation

## Diagnosis: Corticosteroid-Induced Secondary Glaucoma ### Clinical Context This patient has developed glaucoma in the setting of chronic topical corticosteroid use for uveitis management. The open angle on gonioscopy rules out angle-closure mechanisms, and the presence of active inflammation does not fully explain the IOP elevation in isolation. ### Mechanism of Corticosteroid-Induced Glaucoma **Key Point:** Topical corticosteroids increase aqueous outflow resistance, primarily by: 1. Altering trabecular meshwork extracellular matrix composition 2. Increasing glycosaminoglycan deposition in the trabecular meshwork 3. Reducing trabecular cell phagocytic activity 4. Increasing aqueous humor viscosity These changes reduce conventional (trabecular) outflow facility, leading to IOP elevation in susceptible individuals (approximately 30–40% of the population). ### Clinical Pearls **High-Yield:** Corticosteroid-induced glaucoma is dose- and duration-dependent. Potent topical steroids (dexamethasone, betamethasone) carry higher risk than weaker agents (fluorometholone, loteprednol). **Clinical Pearl:** The IOP typically normalizes within 2–4 weeks of corticosteroid discontinuation, confirming the diagnosis retrospectively. **Mnemonic: CIGS** — **C**orticosteroid, **I**ncrease outflow resistance, **G**laucoma, **S**teroid-induced. ### Why This Patient? - Open angle on gonioscopy excludes angle-closure mechanisms - Active uveitis (2+ cells/flare) is present but does not fully account for IOP 38 mmHg - 2-year history of topical corticosteroid use is the critical risk factor - Elevated IOP with open angle + steroid exposure = corticosteroid-induced glaucoma until proven otherwise ### Management 1. Taper and discontinue topical corticosteroids (or switch to weaker agent if uveitis control requires continuation) 2. Initiate topical IOP-lowering medications (prostaglandin analogs, beta-blockers, carbonic anhydrase inhibitors) 3. Monitor IOP and anterior chamber inflammation closely 4. Consider systemic immunosuppression (methotrexate, azathioprine) to control uveitis without prolonged steroid dependence