Uveitic glaucoma presents treatment challenge

Key Points

Editor's Note: Elevated IOP is a common occurrence in patients with uveitis. Management often is quite challenging, however, due to the multiple mechanisms that are at play and the often-countervailing effects of corticosteroids and pressure-lowering agents. We've asked several specialists to comment on their approaches to managing elevated IOP in patients with uveitis, including the use of drops, laser therapy, and surgery.

-Emmett T. Cunningham Jr., MD, PhD, MPH

What is your stepped approach to the use of topical and oral agents in patients with uveitis and elevated IOP? Which class of agents do you use first? How do you choose subsequent agents? Do you try to avoid any agents?

For a patient with uveitis and IOP elevation for the first time, I often would start with an aqueous suppressant in preference to a prostaglandin agonist. If use of a beta-blocker is not contraindicated, then I often would start with that then move on to a beta-blocker/topical carbonic anhydrase inhibitor (CAI) combination if this fails to produce satisfactory control.

I am hesitant to use alpha-agonists and prostaglandin agonists in uveitic patients taking nonsteroidal anti-inflammatory drugs, because there may be some reduction in effect of the former. I also am hesitant to use prostaglandin agonists in uveitic patients unless absolutely necessary because they may confound treatment of active uveitis. On the other hand, I have no hesitation in using them if required.

The uveitic eyes in which I try to avoid prostaglandin agonists include those in patients with a history of macular edema from their uveitis, those in whom the uveitic activity is poorly controlled, aphakic eyes, and those with a history of herpetic keratitis.

Andrew G. Iwach, MD: The initial step in managing uveitic glaucoma is to determine an acceptable target pressure. Many times there is not yet severe optic nerve damage, and so an IOP in the low 20s may be sufficient to preserve vision. Patients who experience elevated IOP only during uveitic episodes may have a good response just to medication.

With uveitic glaucoma, pressures can be erratic and unpredictable. The response to conventional topical ocular hypotensive drugs, likewise, can be highly variable. The eye may respond to minimal drug doses or may not respond at all to high dosing. Lowering IOP medically, if possible, can provide enough time for the inflammation to subside. Corticosteroids may work well for those patients who need episodic control of their IOP in certain circumstances, such as with Posner-Schlossman syndrome or herpetic keratouveitis. Those who have a response to corticosteroids and require long-term systemic corticosteroids to control inflammation often do well taking alternative immunosuppressive drugs, such as methotrexate. If no contraindication is present, typically, beta-blockers would be strongly considered.

Other alternatives would include topical alpha-agonists, such as brimonidine (Alphagan, Allergan), or topical CAIs. Combination drops (for example dorzolamide-timolol [Cosopt, Merck]) sometimes can provide a convenient, effective alternative. In general, prostaglandin analogs can be considered as a second tier. Prostaglandin agonists should be used with caution when there is a history of cystoid macular edema and with particular caution in herpetic keratouveitis. Oral agents may play a role if topical medications prove inadequate. Generally, miotics, for obvious reasons, are avoided in this setting.