Nonpseudophakic Cystoid Macular Edema Medication
- Author: Daniel B Roth, MD; Chief Editor: Hampton Roy, Sr, MD more...
The most common drugs used to treat CME include steroids, nonsteroidal anti-inflammatory drugs (NSAIDs), and acetazolamide.
Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify the body's immune response to diverse stimuli. Used to stabilize the blood-retinal barrier and to induce resolution of macular edema.
Used rarely for severe inflammatory conditions with associated CME. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
Occasionally used in CME; however, poor penetration to the macula via topical route. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
In cases of bacterial infections, concomitant use of anti-infective agents is mandatory; if signs and symptoms do not improve after 2 days, reevaluate patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely.
For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Posterior sub-Tenon injection of steroid to reduce CME. Depending on etiology of edema, it is often DOC.
Dexamethasone is an intravitreal implant used to treat macular edema associated with retinal vein occlusion. The pellet is injected through the pars plana, and through sustained-release, delivers the drug slowly over a month. Increased intraocular pressure and conjunctival hemorrhaging are the 2 main complications associated with the implant.
The fluocinolone acetonide implant uses the drugs low solubility for its sustained-release effect. However, the effect is temporary (results diminish within a year) and risks increases in intraocular pressure. It is FDA-approved to treat certain types of uveitis.
Iluvien, an intravitreal implant with sustained release of fluocinolone acetonide, has been FDA-approved to treat diabetic macular edema.
Nonsteroidal anti-inflammatory agents (NSAIDs)
Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation and various cell membrane functions.
NSAID; often used in conjunction with steroids in treating CME. 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.
NSAID; often used in conjunction with steroids in treating CME. Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclooxygenase, which in turn decreases formation of prostaglandin precursors. May facilitate outflow of aqueous humor and decreases vascular permeability.
Often used in conjunction with steroids in treating CME. 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. Reported to have better penetration into the posterior segment.
Often used in conjunction with steroids in treating CME. 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. Converts from prodrug into active amfenac inside the eye by ocular tissue hydrolases.
Carbonic anhydrase inhibitors
Active in drying macular edema in select situations. Usually of minimal benefit with undesirable systemic side effects.
Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which in turn reduces intraocular pressure (IOP). Second-line drug for CME.
Vascular endothelial growth factor inhibitor
Inhibitor of vascular endothelial growth factor, a potent mediator of angiogenesis and capillary permeability.
Bevacizumab, an inhibitor of vascular endothelial growth factor (VEGF), was approved originally in the treatment of colorectal carcinoma. It is now used commonly via intravitreal injection to treat disorders such as exudative macular edema and retinal vein occlusion.[7, 8] Its use has been reported in treating nonpseudophakic CME as well.
Pegaptanib sodium is a stable RNA aptamer that binds to an isoform of VEGF. It is FDA-approved to treat age-related macular degeneration through intravitreal injection, and is awaiting approval as a treatment for diabetic macular edema. It has also been used with photocoagulation treatment to improve results.
Ranibizumab is an antibody that blocks the entire VEGF family of proteins. It is FDA-approved to treat age-related macular degeneration.
Aflibercept intravitreal is a fusion protein to treat diabetic macular edema, and potentially central retinal vein occlusion. In the DA VINCI study, it was found more effective than laser photocoagulation in showing long-term improvement in visual acuity and reduction in central retinal thickness.
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