This article is more than 5 years old. Information may no longer be current.
Prophylaxis and treatment of cystoid macular edema
Cystoid macular edema is the most common cause of visual decline following cataract surgery. Losses in visual acuity and/or contrast sensitivity due to this complication can be irreversible. However, efficient methods of prophylaxis and treatment are available. This article discusses the best methods for preventing cystoid macular edema and treating patients once it is diagnosed.
Incidence and diagnosis of CME
How common is cystoid macular edema (CME)? Increased retinal thickening is estimated to occur in up to 12% of uncomplicated cataract cases,1 making it about 120 times more likely to occur than postoperative endophthalmitis. Because of its high incidence and the potential for permanent reduced visual function, CME can be considered an even more devastating complication of cataract surgery than endophthalmitis.
Whether angiography or clinical assessment of vision is used as the method of diagnosis, it is important to remember that any change in retinal thickness is significant. Even without visual loss, any evidence of macular retinal thickening should be treated immediately. Optical coherence tomography (OCT) has become a useful tool not only in diagnosing retinal disease, but also in monitoring a patient’s response to therapy.2
Risk factors and etiology
All patients undergoing intraocular surgery are at risk for developing CME, but certain conditions can predispose a patient to this complication. Pre-existing ocular inflammation of any kind is one risk factor, as is diabetes because of the associated vascular incompetence. Macular degeneration, ocular vascular disease and cardiovascular disease are also risk factors. Prophylaxis against CME should be employed in all patients, but it should be started earlier and extended longer in patients deemed to be at high risk.
The pathway leading to CME may involve operative irritation and inflammation, aging, systemic vasculopathy or glaucoma. Whatever the inciting factor, the clinical presentation of CME is the by-product of two processes: the production of prostaglandins in the aqueous and vitreous fluid and the breakdown of the blood-retinal and blood-aqueous barriers.3 Since inhibition of prostaglandin synthesis is known to prevent or reduce ocular inflammation, it presents an excellent target for prophylaxis and treatment of CME.
NSAIDs
NSAIDs have been shown to be an excellent tool for CME prophylaxis and treatment. These agents inhibit the cyclooxygenase pathway, thereby reducing the production of prostaglandins (Figure 1).4 Corticosteroids can be used along with NSAIDs; they inhibit the formation of phospholipase A, an enzyme important to the production of arachidonic acid. Because the two different drugs work on different parts of the inflammatory pathway, they can work together synergistically. Steroids alone, therefore, are not an effective treatment or prophylactic agent for CME.
| NSAIDs Mechanism of Action  Figure 1. NSAIDs inhibit the cyclooxygenase pathway, thereby reducing the production of prostaglandins. Source: Warren KA |
What are the most important characteristics of a CME prophylactic agent? The ideal NSAID would have the ability to penetrate the target intraocular tissues at a therapeutic level; penetrate into the aqueous humor to reduce cell/flare, and penetrate the posterior segment to prevent CME. It would also have excellent analgesic properties and would be a safe and well-tolerated agent.
In a study evaluating the ability of topical nepafenac, diclofenac and ketorolac to prevent the development of induced retinal edema in rabbits, nepafenac was able to significantly reduce the production of prostaglandins (P<.05), resulting in a reduction of markers of inflammation and breakdown of the blood-retinal barrier.5 Neither diclofenac nor ketorolac was able to achieve the same result.
CME treatment
Although preventing CME is the first priority, a surgeon must also be aware of the best methods for treating it when it occurs. The primary treatment is with a topical NSAID and a corticosteroid. For treatment failures, a posterior subtenon corticosteroid injection (20 mg triamcinolone acetonide) in conjunction with a topical NSAID should be administered. Nepafenac penetrates well into the posterior segment and, in my experience with nepafenac given four times a day for 6 weeks, I found it to be effective. This dosage should be tapered to a once-daily dose over the next 6 weeks and maintained for a total of 12 weeks of NSAID therapy. In patients who do not respond to this regimen, an intraocular injection of triamcinolone at 6 weeks may be effective. It is important to remember that some patients will experience permanent visual loss despite long and aggressive treatment, making prophylaxis a critical consideration for any patient undergoing intraocular surgery.
The most frequent complication associated with CME treatment with corticosteroids is increased IOP. It occurs most frequently with the administration of an anterior subtenon injection or with intraocular injection (up to 30% of these patients). Other complications can include cataract formation in phakic patients and vision loss.
In a series of 11 patients I treated who were steroid responders (eight postoperative cataract surgery patients, three macular pucker/CME patients), nepafenac was given four times a day over 6 weeks, and then tapered down over an additional 6 weeks. No patient in this series experienced further visual loss, and eight of 11 had significant visual improvement (two or more lines or 10 ETDRS letters). The other three patients remained stable or had less than a 10-letter improvement.
Furthermore, 10 of the 11 patients had reduced retinal thickness as measured by OCT (mean reduction of 122 µm, range of 55 µm to 276 µm) (Figure 2). There was no correlation, however, between these reductions in retinal thickness and the patient’s final VA.
| OCT Images  Figure 2. Preoperative OCT (top) and postoperative OCT (bottom) of retinal thickness. Following cataract surgery, retinal thickness was reduced in patients who received postoperative nepafenac treatment. Source: Warren KA |
Recommendations and summary
Despite the apparent efficacy of medications to treat patients with CME, the focus should remain on preventing its occurrence. All patients undergoing cataract surgery should be given an NSAID preoperatively as a method of prophylaxis. This can be done up to 3 days preoperatively in low-risk patients and at least 1 week preoperatively in high-risk patients.6
Because CME is the most common cause of visual loss following uncomplicated cataract surgery, this prophylactic regimen should always be kept in mind. If a patient presents with CME postoperatively, the combination of an NSAID and a corticosteroid can provide the best results in treatment. It is important to remember, though, that vision loss is still common even with treatment, so preventing this serious complication should remain the primary goal.
References
- McColgin AZ, Raizman MB. Efficacy of topical Voltaren in reducing the incidence of postoperative cystoid macular edema. Invest Ophthalmol Vis Sci. 1999;40:S289.
- Heier JS. Preventing post-cataract extraction CME: Early identification of patients at risk and prophylactic treatment may avert vision loss. Ophthalmology Management. 2004;63-72.
- Miyake K, Masuda K, Shirato S, et al. Comparison of diclofenac and fluorometholone in preventing cystoid macular edema after small incision cataract surgery: A multicentered prospective trial. Jpn J Ophthalmol. 2000;44:58-67.
- Jampol LM. Pharmacologic therapy of aphakic cystoid macular edema. Ophthalmology. 1982;89:891-897.
- Kapin MA, Yanni JM, Brady MT, et al. Inflammation-mediated retinal edema in the rabbit is inhibited by topical nepafenac. Inflammation. 2003;27:281-291.
- O’Brien TP. Emerging guidelines for use of NSAID therapy to optimized cataract surgery patient care. Curr Med Res & Opin. 2005;21:1131-1137.