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Signs ⬇

Critical

Increased IOP with corticosteroid use. Onset typically 2 to 4 weeks after starting ocular (e.g., topical, intravitreal) steroids, though rarely an acute IOP rise can occur within hours in association with systemic use of steroid or adrenocorticotropic hormone.

Other

Signs of POAG may develop. See 9.1, PRIMARY OPEN-ANGLE GLAUCOMA.

NOTE:

Patients with POAG or a predisposition to development of glaucoma (e.g., family history, ocular trauma, diabetes, African descent, high myopia) are more likely to experience a steroid-response and subsequent glaucoma.

Differential Diagnosis ⬆ ⬇

Etiology ⬆ ⬇

Most commonly seen with ophthalmic topical, periocular, or intravitreal steroid therapy. However, elevated IOP can occur with all forms of administration (e.g., oral, intravenous, inhalational, nasal, injected, or dermatologic topical formulations), especially with prolonged use. More potent topical steroids (e.g., dexamethasone, difluprednate) more often cause significant IOP rises compared to those that are less potent (e.g., fluorometholone, loteprednol). IOP typically decreases to pretreatment levels after stopping steroids. The rate of decrease relates to duration of use and severity of the pressure increase. IOP increase is due to reduced outflow facility of the pigmented TM, and when this is severe, the IOP may remain increased for months after steroids are stopped. IOP increase may also be caused by increased inflammation associated with reduction of the steroid medication.

Work Up ⬆ ⬇

Workup
  1. History: Duration of steroid use? Ask about nasal sprays and dermatologic topical medications. Previous intraocular surgery (possible periocular injection)? Previous steroid use or an eye problem from steroid use? Glaucoma or family history of glaucoma? Herpetic keratouveitis? Diabetes? Myopia? Ocular trauma?
  2. Complete ocular examination: Look for active or prior inflammation and evaluate the iris and angle (by gonioscopy) to determine the presence NV, pigment suggestive of pigment dispersion syndrome or pseudoexfoliation, blood in Schlemm canal, PAS, etc. Inspect the optic nerve.
  3. Complete baseline glaucoma evaluation. See 9.1, PRIMARY OPEN-ANGLE GLAUCOMA.

Treatment ⬆ ⬇

Any or all of the following may be necessary to reduce IOP:

  1. Determine if steroid use (in any form) is truly needed. If not needed, stop or taper steroids.
  2. Reduce the concentration or dosage of steroid.
  3. Change to a steroid with lesser propensity for IOP elevation (e.g., fluorometholone, loteprednol, or rimexolone).
  4. Switch to a topical NSAID (e.g., ketorolac 0.4% or 0.5%, diclofenac 0.1%).
  5. Start antiglaucoma therapy. See 9.7, INFLAMMATORY OPEN-ANGLE GLAUCOMA, for medical therapy options.
  6. Consider anterior chamber paracentesis for rapid control when the IOP is determined to be dangerously high for the involved optic nerve (see Appendix 13, ANTERIOR CHAMBER PARACENTESIS).
  7. LT (e.g., SLT) may be effective in treating some patients.
  8. For sustained IOP elevation after steroid cessation or in patients at risk of glaucoma progression, treat like POAG, including appropriate surgical options. See 9.1, PRIMARY OPEN-ANGLE GLAUCOMA.
NOTE:

For inflammatory glaucoma, if the inflammation is moderate to severe, increase the steroids initially to reduce the inflammation while initiating antiglaucoma therapy.

If a medically uncontrollable dangerously high IOP develops after a depot steroid injection, the steroid may need to be excised. After intravitreal steroid injection, options include glaucoma filtering surgery or a pars plana vitrectomy to remove the steroid.

Steroid-induced glaucoma after LASIK may be difficult to detect using applanation tonometry due to falsely low readings caused by either reduced corneal thickness or interface fluid between the flap and the stromal bed. IOP measurement peripheral to the flap may be more accurate.

Follow Up ⬆

Dependent on severity of pressure elevation and glaucomatous damage. Follow patients as if they have POAG. See 9.1, PRIMARY OPEN-ANGLE GLAUCOMA.