Steroid Induced Glaucoma

Steroid induced glaucoma is secondary open angle glaucoma caused by corticosteroid therapy, through increased outflow resistance in the trabecular meshwork (extracellular matrix deposition, cytoskeleton changes and reduced phagocytosis).

• Occurs with all routes: topical eye drops (most common), periocular and intravitreal injections or implants (triamcinolone, dexamethasone, fluocinolone), oral, inhaled, nasal, dermal (periocular creams), and intravenous.
• Response distribution in general population given 4 to 6 weeks of topical dexamethasone: about 5 percent high responders (rise over 15 mmHg), about 30 percent moderate responders (6 to 15 mmHg), and about 65 percent non-responders.
• High risk groups: primary open angle glaucoma and relatives, high myopia, diabetes, connective tissue disease, children (especially under 6 years), previous steroid responders, angle recession.
• Potency and dose matter: dexamethasone, prednisolone and difluprednate cause more elevation than fluorometholone, loteprednol, and rimexolone.
• Onset usually 2 to 6 weeks after starting, but may be sooner (days) or later (months).

• Often asymptomatic; may present with blurred vision, haloes, mild discomfort, or advanced field loss.
• Intraocular pressure rise (can reach 40 to 60 mmHg), normal angle, normal anterior chamber.
• Corneal oedema in very high pressures; disc cupping in chronic cases.
• Frequently coexists with steroid induced posterior subcapsular cataract.
• Children: asymptomatic until late; consider in any child with chronic steroid use (vernal disease, uveitis, nephrotic syndrome).

• History of steroid use by all routes, duration and potency.
• Tonometry, gonioscopy (open angle), optic disc evaluation, optical coherence tomography and perimetry.
• Rule out other causes: uveitis itself, primary open angle glaucoma, angle recession.
• Monitor pressure at baseline and 2 to 4 weeks after starting a steroid course, then every 3 to 6 months for chronic therapy.

• Stop or reduce the steroid when possible; pressure usually normalises in 1 to 4 weeks (sometimes months, and may not recover in long standing cases).
• Substitute: lower risk steroid (loteprednol 0.5 percent, fluorometholone 0.1 percent), topical NSAID (nepafenac 0.1 percent, ketorolac 0.5 percent), calcineurin inhibitor (ciclosporin 0.05 to 0.1 percent, tacrolimus 0.03 percent ointment), or systemic steroid sparing agent.
• Aqueous suppressants when the steroid is required: timolol 0.5 percent twice daily, dorzolamide 2 percent three times daily, brimonidine 0.2 percent twice daily, prostaglandin analogue at night; acetazolamide 250 mg four times daily for acute rises.
• Intravitreal or periocular depot steroid with high pressure: manage with drops; selective laser trabeculoplasty; remove the implant (dexamethasone implant, fluocinolone) or surgical removal of triamcinolone depot (with vitrectomy) if uncontrolled.
• Laser trabeculoplasty for persistent elevation; trabeculectomy or drainage device for refractory pressure or established damage.
• Surveillance for optic nerve damage, and avoidance of future steroid exposure where possible.
• Counsel patients on risk with over-the-counter steroid eye and skin preparations, and review children on long term steroids every 3 months.