Eyeworld CME Supplements

EW JUL 2013 - Supported by Bausch + Lomb

This is a supplement to EyeWorld Magazine that doctors can take a test after reading and receive CME credits for.

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A third modality for treating inflammation comes from the retinal surgeon's arena. Anti-VEGF therapy uses molecules designed to competitively inhibit the VEGF molecule —which is known to induce endothelial cell vasodilation and promote vascular permeability, leading to vascular leakage and the formation of secondary CME. Indicated for exudative macular degeneration and used off-label to treat a variety of ocular conditions, anti-VEGF therapy is particularly useful in eyes that have had longstanding CME that is unresponsive to other treatment modalities. In cases where first-line treatment with a single agent fails, combination therapy is useful. By combining different modalities— corticosteroids with NSAIDs and/or anti-VEGF therapy—pharmacological intervention occurs at multiple, separate sites of action, allowing for a synergistic effect. Treatment stratification Dr. Warren stratifies his approach to CME treatment according to the duration of the disease. For acute CME occurring 4-6 weeks postop, he uses a combination of a topical steroid and NSAID. For persistent or resistant CME (around 8 weeks postop), he uses a topical steroid or sub-Tenon's injection and an NSAID. For chronic/resistant CME (around 12 weeks postop), he uses an intraocular steroid injection combined with an NSAID. For recalcitrant CME (4-6 months or greater), he would combine an intraocular steroid, an anti-VEGF agent and an NSAID, and may consider vitrectomy and/or a steroid implant. Surgeons should keep in mind that up to 20% of patients treated for CME may rebound after discontinuation of treatment. For such cases, Dr. Warren uses a steroid and an NSAID, with the steroid tapered over 6-8 weeks. But what's really important to keep in mind, said Dr. Warren, is that once CME occurs, the patient will have persistent reduction in contrast sensitivity and color desaturation. "The goal here is to prevent this with prophylaxis," he said. • Acute CME: 4-6 weeks post-op – Treat with topical steroid and NSAID • Persistent or resistant CME (8 weeks or greater) – Treat with topical steroid or sub-Tenon's injection + NSAID • Chronic/resistant CME (12 weeks or greater) – Treat with intraocular steroid injection + NSAID • Recalcitrant CME (4-6 months or greater) – Treat with intraocular steroid + anti-VEGF + NSAID, vitrectomy or perhaps steroid implant • Rebound CME, recurring after discontinuation of topical therapy – Treat with steroid + NSAID, with the steroid tapered over 6-8 weeks Figure 2. CME treatment, stratified by duration of disease chamber; more severe cases may also include significant reduction in vision, as well as pain, redness, and periocular swelling. Postop inflammation, said Dr. Devgan, is "certainly something that we need to treat, especially with premium lenses that require a really quiet eye, good tear film, and no inflammation for the best visual results." "Inflammation slows visual recovery," he added. Fighting inflammation with NSAIDs and steroids together can therefore not only reduce postop inflammation and pain, but also improve visual recovery. Inflammation cascade Several factors influence inflammation after refractive cataract surgery—inherent patient factors such as cataract density, iris color, and the patient's age, as well as surgical factors such as the volume of balanced salt solution run through the eye during surgery and total surgical time. The surgery itself is associated with physical trauma that induces the inflammatory response. Inflammation is the endpoint of the arachidonic acid cascade, which, physiologically, follows the conversion of arachidonic acids into prostaglandins. The cascade thus provides targets for pharmaceutical therapy: Anti-inflammatory medication can block different portions of the pathway, with steroids interfering with the activity of phospholipase A2, thus inhibiting the release of arachidonic acid and arachidonic acid metabolites early in the cascade, and NSAIDs interfering with the activity of COX-1 and COX-2 receptors to inhibit prostaglandin synthesis. Together, steroids and NSAIDs can be used to resolve the anterior chamber cells and flare of inflammation and increase patient comfort. NSAIDs are also used routinely in prophylaxis, administered to prevent inflammation, and while steroids are not used routinely, they can be, said Dr. Devgan. In fact, in his routine preop dosing regimen, Dr. Devgan starts both steroids and NSAIDs together. "If you're going to start with NSAIDs, you may as well start with steroids too," said Dr. Devgan. A logical approach Since inflammation starts immediately, it is logical to get both steroids and NSAIDs into the eye before the first incision. Starting the drugs before the surgery allows the drug to Impact of inflammation on the anterior segment and the role of anti-inflammatory therapy "Inflammation affects the entire eye, front to back," said Uday Devgan, MD, chief of ophthalmology, Olive View UCLA Medical Center, and associate clinical professor, UCLA School of Medicine, Los Angeles. It affects the cornea, the anterior chamber and angle, the iris and ciliary body, the lens capsule, as well as the posterior segment and retina. In the anterior segment, inflammation manifests clinically as hyperemia, miosis, impaired vision, and pain; in the posterior segment, diminished visual acuity may be seen secondary to CME. Postop inflammation typically consists of mild iritis, with clinical signs of ocular inflammation, including cells and flare in the anterior Figure 3. Achieving therapeutic steady state: 1 day vs. 3 days preop

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