CME AFTER CATARACT SURGERY

Effective prevention and treatment of pseudophakic cystoid macular oedema (CME) requires careful surgery that avoids iris trauma in higher risk patients and involves the judicious use of steroids and non-steroidal antiinflammatory drugs (NSAIDs) in all cases, and vitrectomy in certain cases, notes Conceicao Lobo MD, PhD, University Hospital, Coimbra, Portugal. “Correct preoperative evaluation is essential for identifying patients at high risk for CME so that the therapeutic schema can be adapted according to the nature of the patient’s risk,” said Dr Lobo at the 13th EURETINA Congress in Hamburg.

Studies suggest that clinical, symptomatic CME occurs in 0.1 per cent to 2.35 per cent of eyes undergoing cataract surgery when prophylactic measures are taken. Angiographic CME occurs at least 10 times as often. Chronic CME occurs in about one per cent to two per cent of uncomplicated cases and in about eight per cent of complicated cases. The inflammatory condition typically occurs from 4-12 weeks after surgery and its incidence reaches its peak at 4-6 weeks postoperatively. Patients will commonly complain of impaired vision after an initial period of improved vision. OCT examination is usually sufficient to confirm the diagnosis. “In about 90 per cent of patients with macular oedema following cataract surgery, there is a spontaneous resolution of the oedema and recovery of visual acuity. In specific situations there is an excessive leakage that can lead to severe and irreversible impairment of visual acuity, “Dr Lobo said.

Diabetic patients are at an increased risk of CME, especially when they have preexisting diabetic retinopathy. The presence of uveitis may also increase the risk. In some studies the incidence of CME reaches 50 per cent among patients with uveitis associated with juvenile rheumatoid arthritis or pars planitis. Other reports suggest uveitis carries a less elevated risk.

Certain surgical complications can also raise the risk of CME. They include rupture of the posterior capsule, vitreous loss or incarceration, iris trauma, dislocated IOL, retained lens fragments and YAG laser capsulotomy. Lengthy cataract procedures, even when uneventful, can also increase the risk for the complication. The prevention and treatment of pseudophakic CME is centred on the use of drugs that block the inflammatory mediators released in response to surgical trauma. Treatment with corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs) appear to have a synergistic effect on CME. Corticosteroids interfere with the activity of phospholipidase A, thereby selectively inhibiting Cox-2, and NSAIDs inhibit both Cox-1 and Cox-2.

All cataract patients should routinely receive postoperative topical steroids and NSAIDs. Patients should instill the steroid drops, prednisolone or dexamethasone, five times a day during the first postoperative week and three times a day during the second and third postoperative week. They should use topical NSAIDs 2-4 times a day (depending on the NSAID used) during the first postoperative week then 2-3 times a day for the following four postoperative weeks.

As an additional prophylaxis against pseudophakic CME, patients at high risk for the complication should receive topical steroids and NSAIDs preoperatively and patients receiving prostaglandin analogues should replace them with another IOPlowering agent.

“There is some controversy regarding the optimal regimen for prophylaxis of CME. Given the low incidence of CME, it is not possible to prove scientifically what the best schema is. However, data from the large multicentred randomised PREMED study, led by University of Maastricht and funded by ESCRS, once completed, should provide some clarity and enable us to standardise these protocols.”

There is less controversy regarding the treatment of CME. The results of randomised clinical trials show that steroids and NSAIDs improve visual acuity and have a synergistic effect. Therefore, the currently recommended regimens for the treatment of clinical CME are to administer topical steroids and NSAIDs four times a day for one month. If there are improvements in visual acuity and OCT, the treatment should be continued for another two months.

If there is no improvement, the possible next step is to add acetazolamide to the regimen at a dosage of 500mg a day for four weeks, first isolated or together with a sub-Tenon’s injection of 40mg of triamcinolone. If there is then a response, the triamcinolone injection should be repeated two or three times over a period of 3-6 weeks. If there is still a poor response then consider injecting triamcinolone intravitreally at a dosage of 4mg.

Some new treatments now under investigation include anti-VEGF and immunomodulatory therapy. Both require further evaluation to precisely determine their therapeutic value in eyes with CME, Dr Lobo said. Vitrectomy is a useful option in the treatment of CME in some of the more complicated cataract cases. Such cases include those with pupillary or IOL distortion or prolapse, eyes with vitreous incarceration and retained led fragments, and those where vision continues to decline despite pharmacological therapy.

“The rationale for performing vitrectomy in cases with CME following cataract surgery is that it enables the removal of vitreous adhesions and inflammatory mediators and also allows improved access of topical medication to the back of the eye,” Dr Lobo added.

Conceição Lobo: clobofonseca@gmail.com