Steroid-Induced Glaucoma

Steroid-induced glaucoma is intraocular pressure elevation caused by corticosteroid use, occurring through any route, topical, periocular, intravitreal, or systemic, and capable of causing genuine, permanent optic nerve damage if it goes unrecognized.

Because corticosteroids are prescribed so widely, for ocular inflammation, after intraocular surgery, and for a long list of systemic conditions, steroid-induced glaucoma is a hazard that essentially every ophthalmologist and many other prescribers need to keep in mind by default.

The fact that it is entirely iatrogenic and frequently reversible if caught early, but not always if caught late, is what makes surveillance so worthwhile.

Roughly a third to a half of the general population shows at least a modest pressure rise with sustained potent topical steroid exposure, and a smaller subset shows a much more pronounced response, which is why every patient on steroids deserves individualized monitoring rather than a one-size-fits-all assumption.

Mechanism

Corticosteroids increase resistance to aqueous outflow through the trabecular meshwork, thought to involve accumulation of extracellular matrix material and altered trabecular meshwork cell function under sustained steroid exposure.

This mechanism is distinct from the mechanisms behind most other secondary glaucomas, and pressure elevation typically develops gradually over weeks of steroid exposure rather than appearing immediately after the first dose.

Susceptibility varies considerably between individuals: a subset of the population, termed steroid responders, develop significant pressure elevation with even modest steroid exposure, while others tolerate sustained, higher-dose steroid treatment with minimal pressure change.

Risk Factors for Being a Steroid Responder

A personal or family history of primary open-angle glaucoma, one of the strongest known predictors of a significant steroid response
High myopia, also associated with increased susceptibility to steroid-induced pressure elevation
Younger age, particularly in children, who tend to mount a more pronounced and sometimes more rapid steroid response than adults
Diabetes mellitus, associated with somewhat increased steroid responsiveness in some studies
Prior documented steroid response, the single most reliable individual predictor of a repeat response with future steroid exposure

Route Matters

Topical corticosteroid drops carry the most familiar and well-studied risk, with potency, dosing frequency, and duration of treatment all influencing how likely and how severe a pressure response will be.

Periocular and intravitreal steroid injections and implants can produce more pronounced, sometimes more prolonged pressure elevation than topical drops, in part because they deliver a sustained, higher local drug concentration directly to periocular and intraocular tissue.

Systemic corticosteroids, whether oral, inhaled, or intranasal, carry a real but generally lower risk of clinically significant intraocular pressure elevation compared to direct ocular exposure, though the risk is not zero and should not be forgotten in a patient on long-term systemic steroid therapy.

Clinical Presentation and Evaluation

Steroid-induced glaucoma is typically asymptomatic in its early stages, exactly like primary open-angle glaucoma, which is why routine pressure monitoring during any significant steroid course matters rather than waiting for symptoms to prompt a check.

Any patient started on a meaningful course of topical, periocular, or intravitreal steroid should have intraocular pressure checked at baseline and again within a few weeks, since most steroid responses become apparent within the first four to six weeks of treatment.

Gonioscopy is typically normal, since steroid-induced glaucoma is an open-angle process, which helps distinguish it from angle-closure mechanisms and confirms that the pressure elevation is specifically related to trabecular outflow resistance.

Optic nerve and visual field assessment should follow the same standard glaucoma workup used for any other cause of elevated pressure, since the nerve does not distinguish steroid-induced pressure elevation from any other source of damage.

Management

Discontinuing or tapering the causative steroid, when clinically feasible, is the most direct treatment, and pressure often normalizes over subsequent weeks once steroid exposure stops, particularly if the steroid course was relatively brief.

When steroid therapy cannot be discontinued because the underlying inflammatory condition still requires treatment, switching to a lower-potency steroid, a steroid with a more favorable pressure profile, or a non-steroidal anti-inflammatory alternative can reduce the pressure burden while still controlling inflammation.

Standard topical glaucoma medications are used to control pressure directly when steroid therapy must continue, following the same treatment principles used for primary open-angle glaucoma.

Pressure elevation from long-acting intravitreal steroid implants can be more difficult to manage medically given the sustained drug depot, and some cases ultimately require incisional glaucoma surgery if pressure remains uncontrolled despite maximal medical therapy.

Once a patient is identified as a documented steroid responder, that fact belongs clearly in their chart, since it should influence how cautiously any future steroid course, ocular or otherwise, is monitored going forward.

References

Armaly MF. Statistical attributes of the steroid hypertensive response in the clinically normal eye. Investigative Ophthalmology.
American Academy of Ophthalmology. Basic and Clinical Science Course, Section 10: Glaucoma.
Kersey JP, Broadway DC. Corticosteroid-induced glaucoma: a review of the literature. Eye.

Steroid-Induced Glaucoma: The Pressure Rise Prescribers Forget to Check