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Nonpseudophakic Cystoid Macular Edema Medication

  • Author: Daniel B Roth, MD; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Aug 21, 2014
 

Medication Summary

The most common drugs used to treat CME include steroids, nonsteroidal anti-inflammatory drugs (NSAIDs), and acetazolamide.

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Corticosteroids

Class Summary

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.

Prednisone (Deltasone, Orasone, Meticorten)

 

Used rarely for severe inflammatory conditions with associated CME. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Prednisolone acetate 1% ophthalmic solution (Pred Forte)

 

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.

Triamcinolone (Amcort, Kenalog)

 

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 (Posurdex)

 

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.

Fluocinolone acetonide (Retisert, Iluvien)

 

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.

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Nonsteroidal anti-inflammatory agents (NSAIDs)

Class Summary

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.

Ketorolac ophthalmic (Acular)

 

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.

Diclofenac ophthalmic (Voltaren)

 

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.

Bromfenac ophthalmic (Xibrom)

 

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.

Nepafenac ophthalmic (Nevanac)

 

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.

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Carbonic anhydrase inhibitors

Class Summary

Active in drying macular edema in select situations. Usually of minimal benefit with undesirable systemic side effects.

Acetazolamide (Diamox)

 

Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which in turn reduces intraocular pressure (IOP). Second-line drug for CME.

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Vascular endothelial growth factor inhibitor

Class Summary

Inhibitor of vascular endothelial growth factor, a potent mediator of angiogenesis and capillary permeability.

Bevacizumab (Avastin)

 

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 (Macugen)

 

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 (Lucentis)

 

Ranibizumab is an antibody that blocks the entire VEGF family of proteins. It is FDA-approved to treat age-related macular degeneration.

Aflibercept intravitreal (Eylea)

 

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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Contributor Information and Disclosures
Author

Daniel B Roth, MD Assistant Professor, Department of Ophthalmology, Retina Vitreous Center, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School

Daniel B Roth, MD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Society of Retina Specialists, Retina Society, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Howard F Fine, MD, MHSc Partner, Associated Retina Consultants, Retina Vitreous Center, PA; Co-founder and Chairman of Scientific Advisory Board, Auris Surgical Robotics, Inc

Howard F Fine, MD, MHSc is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, Association for Research in Vision and Ophthalmology, American Society of Retina Specialists

Disclosure: Nothing to disclose.

Tahia Haque University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School

Disclosure: Nothing to disclose.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Steve Charles, MD Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Macula Society, Retina Society, Club Jules Gonin

Disclosure: Received royalty and consulting fees for: Alcon Laboratories.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

V Al Pakalnis, MD, PhD Professor of Ophthalmology, University of South Carolina School of Medicine; Chief of Ophthalmology, Dorn Veterans Affairs Medical Center

V Al Pakalnis, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, South Carolina Medical Association

Disclosure: Nothing to disclose.

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Fundus photograph of left eye with branch retinal vein occlusion and cystoid macular edema. Visual acuity was 20/50, and the patient was treated with a modified grid laser photocoagulation and posterior sub-Tenon injection of triamcinolone.
Fundus photograph of nonproliferative diabetic retinopathy with clinically significant macular edema and cystoid macular edema.
Fluorescein angiogram of same eye as in the image above, revealing both cystoid macular edema and leakage from microaneurysms associated with diabetic retinopathy.
Ocular coherence tomographic image of cystoid macular edema in a patient with uveitis.
Cystoid macular edema in patient with diabetic retinopathy.
Eye in previous image with diabetic CME after injection with 4 mg of intravitreal triamcinolone.
Ocular coherence tomographic image of cystoid macular edema in an eye with nonproliferative diabetic retinopathy.
 
 
 
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