Cystoid macular edema (CME) following cataract surgery has been recognized for over 50 years as an important cause of suboptimal post-operative vision. The incidence of CME varies widely, but is likely in the range of 1-2% using modern cataract extraction techniques. The diagnosis of CME can generally be made on clinical examination with evidence of perifoveal cystic spaces and can be confirmed with use of fluorescein angiography to document the classic petaloid pattern of leakage mainly into the outer retina. Leak from perifoveal vessels is induced by inflammatory mediators and results in intraretinal fluid accumulation and corresponding decrease in retinal function. The risk factors most associated with CME; rupture of posterior capsule, vitreous loss, iris incarceration, use of iris fixated lenses, active uveitis and diabetes, may all increase the potency of these mediators and exacerbate post-operative CME. The treatment of CME remains controversial but generally starts with conservative observation in isolated angiographic cases and progresses through topical non-steroidal anti-inflammatory agents (NSAIDs), topical steroids, peri-ocular steroids, systemic steroids and surgical intervention in refractory cases. Even more controversial is the role of NSAID prophylaxis peri-operatively in preventing clinical CME. Though the data is tantalizing in the short term, there is little to support the long-term benefit of such prophylaxis with respect to visual outcomes.
