Steroid-induced glaucoma is a unique and often challenging problem. To begin with, elevated intraocular pressure (IOP) in the setting of topical steroid use can be challenging from a diagnostic standpoint, as many of the conditions that necessitate steroid use, e.g., post-surgical inflammation or uveitis, can themselves induce elevated IOP.
The epidemiology of the steroid response deserves some consideration. About 5% of the population would be considered a high steroid responder, and steroid response follows a bimodal distribution, disproportionately affecting the very young and the older population.1 Patients with a personal or family history of glaucoma are much more likely to exhibit a steroid response. The route of administration of the agent will affect the likelihood of response, with topical and systemic administration being less likely to induce a response compared to intravitreal steroid administration, where as many as half of injected patients may see a pressure response. The duration of administration is key component as well, and some data suggests that three-quarters or almost all patients will eventually develop some intraocular pressure elevation if treated with a high enough dose for a long enough period of time. In the multicenter uveitis steroid treatment trial, 70% of patients receiving a fluocinolone acetonide intravitreal implant required IOP-lowering therapy.2 In general, the likelihood of the pressure response is directly proportional to the efficacy of the agent’s anti-inflammatory properties. Additionally, patients who have responded to a steroid response previously often will respond again, and having received a course of steroid without a pressure elevation makes a future steroid response less likely.
The typical patient with a steroid-related IOP rise usually has a few positive prognostic features. These patients typically do not have pre-existing optic nerve damage, and additionally may not have a nerve that is particularly susceptible to elevated IOP. Medications can reduce the pressure very well, and most-often the first line agent would be a fixed combination because of their strong efficacy and to avoid any potential concerns regarding inflammation associated with prostaglandin analogues.
Selective laser trabeculoplasty may have better than average efficacy in a steroid-induced glaucoma population, with one series reporting 30-50% IOP lowering up to 6 months after the laser.3 Finally, glaucoma filtration surgery may work particularly well in this population as the steroid may inhibit an exuberant wound healing response that can lead to failure. Fortunately, for the majority of patients who are being treated with topical steroids, the need for the medication is short-lived, and tapering off the offending agent (or excising it in the case of sub-tenon triamcinolone) will lead to a resolution of the elevated intraocular pressure.
In summary, steroid-induced glaucoma is a unique secondary glaucoma with its own features. Knowing the playbook of this type of glaucoma can help the clinician.
1. Razeghinejad MR, Katz LJ. Steroid-induced iatrogenic glaucoma. Ophthalmic Res. 2012;47(2):66-80.
2. Friedman DS, et al. Risk of elevated intraocular pressure and glaucoma in patients with uveitis: results of the multicenter uveitis steroid treatment trial. Ophthalmology. 2013 Aug;120(8):1571-9.
3. Rubin B, et al. The effect of selective laser trabeculoplasty on intraocular pressure in patients with intravitreal steroid-induced elevated intraocular pressure. J Glaucoma. 2008 Jun-Jul;17(4):287-92.
Dr. Nathan M. Radcliffe is the director of the glaucoma service and a clinical assistant professor at
New York Univeristy Langone Ophthalmology Associates and is a cataract and glaucoma surgeon at
the New York Eye Surgery Center.