Anand Mantravadi



Steroid-induced glaucoma is a secondary open-angle glaucoma that results after the use of local or systemic corticosteroids. Intraocular pressure (IOP) increase results from decreased aqueous humor outflow facility. Glaucomatous optic neuropathy can then develop from this ocular hypertension.



• Incidence of IOP rise varies with route of administration, formulation of medication, and total cumulative dose.

• 5% of people treated with topical steroids for 4–6 weeks show an IOP rise of ≥16 mm Hg, 30% show an IOP rise of 6–15 mm Hg

• Intravitreal > periocular > topical > systemic

• Intravitreal triamcinolone acetonide (4 mg)—14.6–44.6%

• Prednisolone acetate (1%)—6.7%

• Loteprednol etabonate (0.2 and 0.5%)—1.7%

• Case reports with inhaled, intravenous, oral, and topical corticosteroid use




• Diagnosis of primary open-angle glaucoma

• First-degree relative with primary open-angle glaucoma

• High baseline IOP

• Traumatic angle recession

• High myopia

• Connective tissue disease

• Type 1 diabetes mellitus

• Children

• Elderly


• No clear genetic component

• Myocilin may be overexpressed by meshwork cells when exposed to steroids and myocilin gene mutations have been associated with juvenile and adult-onset glaucomas.


• Be aware of those populations at risk.

• Limit exposure to necessary corticosteroids.

• Use formulations less likely to cause IOP rise.


• Decreased aqueous humor outflow facility

• Possible architectural changes of the trabecular meshwork (i.e., actin crosslinking)

• Possible deposition of material in the trabecular meshwork (i.e., glycosaminoglycans)

• Possible decreased phagocytic function of trabecular meshwork cells with decreased ability to remove material accumulated in the meshwork




Any requiring use of corticosteroids



• Patient being treated with topical or systemic corticosteroids. Do not forget to inquire about depositions (intravitreal, periocular) or inhalational, intranasal, or dermatologic formulations. Attempt to identify those patients that are at higher risk of developing elevated IOP with steroid use.

• Presentation may be within 1 week of initiating therapy but may be delayed up to years later.

• Typical time to presentation for ophthalmic drop formulations is 3–8 weeks


• IOP elevated from baseline

• If asymmetric optic nerve damage exists, there may be a relative afferent pupillary defect

• Slit lamp exam will likely be within normal limits or no change from patient baseline

• Gonioscopy will be consistent with patient baseline

• Examination of the optic nerve may show evidence of typical glaucomatous damage (diffuse narrowing of the neuroretinal rim, focal notches, disc hemorrhage). Prior glaucomatous damage makes the nerve more susceptible to further damage at lower IOP increases for shorter durations.



Optic nerve head imaging (i.e., confocal scanning laser ophthalmoscopy) or retinal nerve fiber layer imaging (optical coherence tomography or scanning laser polarimetry) may be used in conjunction with optic nerve exam to evaluate for glaucomatous damage.

Diagnostic Procedures/Other

• Standardized visual fields should be obtained to assess for evidence of glaucomatous functional deficits.

• Pachymetry

Pathological Findings



• Primary open-angle glaucoma

• Uveitic glaucoma



First Line

• Cessation of steroids if possible. Tapering to a lower dose can ultimately result in reduction in pressure.

• Beta-adrenergic antagonists (topical)

– Timolol maleate 0.25–0.5%, one drop daily or b.i.d.

– Betaxolol 0.25%, one drop b.i.d.

• Alpha2-adrenergic agonists (topical)

– Brimonidine tartrate 0.15%, one drop b.i.d. or t.i.d.

• Carbonic anhydrase inhibitors (topical)

– Dorzolamide 2.0%, one drop b.i.d. or t.i.d.

– Brinzolamide 1%, one drop b.i.d. or t.i.d.

• Prostaglandin analogues/prostamides (topical)

– Latanoprost 0.005%, one drop qHS

– Travoprost 0.004%, one drop qHS

– Bimatoprost 0.03%, one drop qHS

• Combinations (topical)

– Dorzolamide/timolol maleate 2%/0.5%, one drop b.i.d.

– Brimonidine tartrate/timolol maleate 2%/0.5%, one drop b.i.d.

Second Line

• Carbonic anhydrase inhibitors (systemic)

– Acetazolamide 125–250 mg po b.i.d. to q.i.d.

– Acetazolamide sequels 500 mg po b.i.d.

– Acetazolamide (parenteral) 500 mg IV once daily or 5–10 mg/kg q6–8h

– Methazolamide 50–100 mg po b.i.d. to t.i.d.

• Hyperosmotic agents

– Mannitol 20% solution, 0.5–2 mg/kg IV infused over 30–60 minutes (20% solution has 20 g per 100 mL)


Additional Therapies

Selective laser trabeculoplasty (SLT) may be effective in some patients. One must consider the potential for IOP rise after SLT and the urgency in which the patient’s IOP must be lowered.


• Trabeculectomy with antifibrotic agents (mitomycin C)

• Aqueous drainage device implantation (Baerveldt shunt, Ahmed valve, Molteno implant, etc.)



• Patients should be followed closely after the administration of steroids, especially those receiving intravitreal, periocular, and topical formulations.

• Appropriate follow-up has been suggested to be 2 weeks after steroids are administered. Patients determined to be at higher risk should be examined sooner and more often (after 1, 4, and 8 weeks).

• Generally, lowering IOP below 30 mm Hg is a reasonable goal for individuals without optic nerve damage.

• Preexisting or newly diagnosed glaucomatous damage to the optic nerve warrants more aggressive treatment. In general, IOP should be maintained at or below target IOP as determined in glaucoma patients before starting steroids.

Patient Monitoring

• Serial examinations in which visual function, IOP, and optic nerve are evaluated

• Repeat visual fields as necessary


Patients should be counseled on their risk of IOP rise and the potential of irreversible vision loss via optic nerve damage before implementation of therapy.


Prognosis depends on level of IOP rise and amount of optic nerve damage. With regular monitoring and appropriately aggressive therapy, loss of visual function can frequently be avoided.


• Visual field constriction

• Vision loss


1. Spaeth GL, de Barros M, Fudemberg S.Retina 2009;29(8):1057–1061.

2. Jones R III, Rhee D.Curr Opin Ophthalmology 2006;17(2):163–167.

3. Stamper R, Lieberman M, Drake M.Becker-Shaffer’s diagnosis and therapy of the glaucomas. 270–271.

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Nov 9, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Glaucoma

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