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Importance of addressing cystoid macular edema
Fifth in a series of the top 10 reasons for poor premium IOL outcomes and how to remedy them.
The etiology of visual loss in cataract surgery can be multifactorial, including but not exclusive to ocular surface disease, such as dry eye, blepharitis, allergy and epithelial basement membrane dystrophy; regular and irregular astigmatism; keratoconus and forme fruste keratoconus; pre-existing retinal pathology, such as epiretinal membrane, age-related macular degeneration and diabetic retinopathy; posterior capsular opacification; and cystoid macular edema.
Any of these problems becomes even more magnified in a premium patient paying premium prices for premium IOL technology. Astigmatism and PCO management were addressed in the third and fourth part of this 10-part series, and ocular surface disease will be addressed in the next issue.
Diagnosing CME
Cystoid macular edema (CME) is the most common cause of significant visual loss in patients without pre-existing disease and was readily underdiagnosed until more frequent use of postoperative optical coherence tomography testing began allowing for earlier detection. The current definition of CME includes an ophthalmic appearance of a cystic yellow fovea, petaloid leakage on fluorescein angiography, any visual deficit including metamorphopsia and decreased contrast sensitivity.
Angiography is the gold standard, but Flach has published that macular thickening correlates better with vision loss, and visual acuity does not always correlate with degree of angiographic leakage. Angiography is useful, however, to confirm the presence or absence of CME. OCT provides a much faster, easier, safer and even better look at retinal structure and is especially helpful for determining preoperative retinal pathology, such as epiretinal membrane, age-related macular degeneration and diabetic retinopathy, and postoperative CME diagnosis and monitoring of therapeutic response.
Onset of CME is typically not seen until around 4 to 6 weeks postoperatively. Pathophysiology of CME includes inflammation, surgical trauma of ocular tissue, retained lens fragments, vitreous traction, photic toxicity and possibly pharmacology (epinephrine, tamoxifen). High-risk patients include diabetics (even without diabetic retinopathy), as well as those with previous central or branch retinal vein occlusion, epiretinal membranes, uveitis history, previous CME, CME in fellow eye, previous ocular surgery and prolonged operative time. The decision to perform premium IOL surgery should be reassessed based on a patient’s risk factors to develop CME.
Treatment
Treatment of CME can be primarily addressed based on the inflammation etiology model: Topical steroids and NSAIDs work synergistically at the arachidonic acid cascade level to reduce inflammation. NSAIDs primarily act on the cyclooxygenase pathway (COX-1 and COX-2) by decreasing prostaglandin formation, and steroids act on phospholipase A2 by decreasing arachidonic release.
There are a number of U.S. Food and Drug Administration-approved NSAIDs and steroids for pain and inflammation after cataract surgery, including Bromday (bromfenac ophthalmic solution 0.09%, Ista Pharmaceuticals), Acuvail (ketorolac tromethamine ophthalmic solution 0.45%, Allergan), Nevanac (nepafenac ophthalmic suspension 0.1%, Alcon) and Durezol (difluprednate ophthalmic emulsion 0.05%, Alcon).
A large prospective, randomized, double-masked, multicenter trial showed statistically significant less clinical CME and less mean retinal thickening on OCT in patients taking NSAIDs and steroids combined vs. steroids alone in low-risk patients — those typically receiving premium IOL technology. In my premium IOL patients (low-risk CME cases), I begin topical NSAID therapy 3 days before surgery and continue it 4 weeks postoperatively.
OCT is an excellent way to guide withdrawal of NSAID therapy. I always perform OCT at the 1-month postoperative visit to be sure there are no subtle CME changes prior to NSAID withdrawal. The main precaution with topical NSAID therapy is to avoid usage in patients with severe dryness and/or unstable autoimmune disease so as to avoid corneal melts. These latter patients are not typically candidates for premium IOL technology, anyway. With patients who typically develop CME that is unresponsive to steroid-NSAID combination therapy, referral to a retinal specialist for intravitreal steroid and/or anti-VEGF therapy may be indicated.
Recognizing high-risk CME patients, efficient cataract surgery and prophylactic topical NSAID usage will regularly give your premium patients a visual outcome free of CME.
Stay tuned for managing the ocular surface in your premium IOL patient in the January/February 2012 issue.
References:
Flach AJ. The incidence, pathogenesis and treatment of cystoid macular edema following cataract surgery. Trans Am Ophthalmol Soc. 1998;96:557-634.
Wittpenn JR, Silverstein S, Heier J, Kenyon KR, Hunkeler JD, Earl M; Acular LS for Cystoid Macular Edema (ACME) Study Group. A randomized, masked comparison of topical ketorolac 0.4% plus steroid vs steroid alone in low-risk cataract surgery patients. Am J Ophthalmol. 2008;146(4):554-560.
Mitchell A. Jackson, MD, can be reached at Jacksoneye, 300 N. Milwaukee Ave., Suite L, Lake Villa, IL 60046; 847-356-0700; fax: 847-589-0609; email: mjlaserdoc@msn.com.
Disclosure: Dr. Jackson is on the speakers bureau for Ista, Allergan and Alcon.