Steroid-Induced Glaucoma

The trabecular meshwork is a sieve-like structure at the iridocorneal angle through which most aqueous humor drains. Its cells are metabolically active and responsive to corticosteroids, which is the anatomical basis for steroid-induced glaucoma — a secondary open-angle glaucoma resulting from corticosteroid-induced ocular hypertension that, if unrecognized or prolonged, progresses to glaucomatous optic nerve damage.¹

Steroid-induced ocular hypertension arises from increased trabecular meshwork outflow resistance, primarily through decreased matrix metalloproteinase expression, promoting abnormal extracellular matrix deposition and trabecular meshwork cell dysfunction.¹ Steroid-induced actin cytoskeleton changes increase trabecular meshwork stiffness, and elevated MYOC (myocilin) gene expression has been observed with steroid exposure.¹ The glucocorticoid receptor beta isoform (GRβ) normally acts as a dominant-negative regulator of glucocorticoid activity; trabecular meshwork cells from POAG eyes show lower GRβ expression than controls, providing a plausible mechanism for the much higher steroid-response rate in POAG patients specifically.²

Steroid-induced glaucoma is typically asymptomatic in early stages and identified through IOP monitoring in a patient on steroid therapy, rather than patient-reported symptoms. A history of any steroid exposure — topical, periocular, intravitreal, inhaled/intranasal, or systemic — should be specifically elicited in any patient with unexplained ocular hypertension. Gonioscopy shows an open angle, consistent with a secondary open-angle mechanism.

Differential diagnosis includes coincidental primary open-angle glaucoma diagnosed during steroid treatment, uveitic glaucoma from the underlying inflammatory condition being treated (can coexist and be hard to distinguish), and other secondary open-angle glaucomas (pigmentary, pseudoexfoliative).

In patients requiring prolonged steroid therapy, especially those with known glaucoma risk factors, a short topical steroid 'challenge' — a brief trial course with IOP monitoring — has shown moderate predictive value for anticipating IOP response to subsequent, more prolonged exposure (such as an intravitreal implant), supporting tailored monitoring for higher-risk patients.³ Ongoing IOP monitoring throughout any steroid course, including after multiple prior uneventful doses, is essential, since delayed ('late') responses can occur.

The most direct management once steroid-induced ocular hypertension is identified is discontinuing or reducing the steroid — switching to lower potency, less frequent dosing, or a non-steroidal alternative — if the underlying condition allows. When continued steroid therapy is necessary, standard IOP-lowering medical therapy is used, following the same principles as POAG management.

Most steroid-induced ocular hypertension is reversible if the steroid is discontinued and treatment duration was under approximately one year, though prolonged, unrecognized exposure can cause permanent optic nerve damage and vision loss.¹

• Almost all POAG patients are steroid responders, compared with about 40% of the general population — always ask about glaucoma history before or during steroid therapy
• IOP elevation is usually reversible if steroid exposure is under about a year — but timely recognition is essential
• Late steroid-response IOP spikes can occur even after several prior uneventful intravitreal steroid injections — don't relax monitoring after early doses are well tolerated
• Common pitfall: failing to ask about all forms of steroid exposure (topical, inhaled, intranasal, systemic) in unexplained ocular hypertension
• Common pitfall: abruptly discontinuing necessary steroid therapy for IOP control without arranging adequate alternative management of the underlying condition