Summary: Though CME was first described nearly 50 years ago, it remains a majorcause of sub-optimal vision following cataract surgery in a significant number of patients.There does not appear to be a statistically different rate of clinical CME between ECCEand phacoemulsification techniques. The major pathology is postoperative inflammationthat stimulates breakdown of the blood-ocular barrier and subsequent leakage intoperifoveal retinal tissues. The incidence of clinical CME is likely in the range of 0.2 to 2%.The rate of angiographic CME is ten-fold higher. The vast majority of cases fromuncomplicated surgeries show spontaneous resolution of CME. However, some patientsdevelop chronic form. Fluorescein angiography is the gold standard for diagnosis, whileOCT offers precise measurement for axial thickness. NSAIDs are effective in the treatmentof clinical and angiographic CME in uncomplicated cases. Steroids appear to be effectivewhen treating patients with evidence of anterior segment inflammation and followingposterior capsular trauma. There are several formulations, and a stepwise plan may beundertaken. Vitrectomy is an effective treatment in cases where there is evidence ofanterior segment pathology. Anti VEGF treatment is promising. Most surgeonsrecommend that long-term medical prophylaxis be attempted before surgical interventionis entertained as well as preoperative control of intraocular inflammation, diabetes, andblood pressure in susceptible patients.Results: Pseudophakic macular edema remains an important issue, despite lower incidencewith emerging cataract surgery techniques. The treatment of this condition is medical withpromising results shown with intravitreal injection of steroids and posterior segmentsustained release devices.