Pseudophakic (Irvine-Gass) Macular Edema Medication

Updated: Sep 25, 2018
  • Author: David G Telander, MD, PhD; Chief Editor: Michael Taravella, MD  more...
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Medication

Medication Summary

Medical therapy of Irvine-Gass syndrome includes NSAIDs, corticosteroids, and carbonic anhydrase inhibitors.

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Nonsteroidal anti-inflammatory drugs

Class Summary

NSAIDs inhibit enzyme cyclooxygenase and also can be used in the prevention of CME. NSAIDs are administered topically, usually for 3-4 months. This class of drops have not been thought to cause elevated IOP (glaucoma) or cataract formation.

Diclofenac ophthalmic (Voltaren)

Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclooxygenase, which in turn decreases formation of prostaglandin precursors. Commonly used in the treatment of CME and for postoperative inflammation in patients who have undergone cataract extraction.

Ketorolac ophthalmic (Acular)

Inhibits prostaglandin synthesis by decreasing activity of the enzyme, cyclooxygenase, which results in decreased formation of prostaglandin precursors, which in turn results in reduced inflammation.

Nepafenac (Nevanac, Ilevro)

Nepafenac is a pro-drug of amfenac, a potent NSAID. Nepafenac undergoes amide hydrolysis by intraocular hydrolases to form the pharmacologically active amfenac. Amfenac inhibits both cyclooxygenase COX-1 and COX-2 activity. Therefore, its effects are intraocular (CME) and have less effect (or side-effect) on the ocular surface.

Bromfenac ophthalmic (Prolensa)

This new NSAID blocks prostaglandin synthesis by inhibiting cyclooxygenase 1 and 2 and is unique in its once-a-day dosing and effective penetration to the posterior pole.

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Carbonic anhydrase inhibitors

Class Summary

Carbonic anhydrase is present on both the apical and basal surfaces of the RPE cell membrane. CAIs enhance the pumping action of RPE cells and change ion flux, which affects the cellular environment in the retina.

Acetazolamide (Diamox)

Facilitates the transport of water across the retinal pigment epithelium from the subretinal space to the choroid. Has been found to be useful in cases of CME, but is more commonly used for lowering IOP in the therapy of glaucoma.

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Corticosteroids

Class Summary

Inhibit the enzyme phospholipase and have a primary role in treatment of CME secondary to uveitis. Can be administered topically, orally, or injected in the sub-Tenon space.

Prednisolone acetate (Omnipred, Pred Forte, Pred Mild)

Indicated in several conditions of steroid-responsive intraocular inflammation including CME.

Triamcinolone intravitreal (Triesence)

Indicated in several conditions of steroid-responsive intraocular inflammation and CME.

Dexamethasone intravitreal implant (Ozurdex)

Indicated in several conditions of steroid-responsive intraocular inflammation and CME. Approved for macular edema in patients with diabetes.

Prednisolone (FloPred, Millipred, Millipred DP, Prelone)

Prednisolone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN) leukocyte activity. It is a commonly used oral agent. Prednisolone is used for an oral taper of steroids, which may reduce the emotional effects of steroid withdrawal and the risk of the development of adrenocortical insufficiency.

Triamcinolone (Aristospan, Kenalog)

Triamcinolone is used in the treatment of inflammatory disorders responsive to steroids. It decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Dexamethasone (Dexamethasone Intensol)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

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