Cystoid macular edema (CME) is characterized by cystoid spaces in the macular area with perifoveal fluorescein leakage, increased thickness of the retina, and visual impairment. This form of CME is referred to as clinically significant CME. CME can also be present without the increased macular thickness and is referred to as angiographic CME (1, 2, 3, 4 and 5). CME is not a frequent complication of recent, modern, and successful cataract extraction and posterior intraocular lens (IOL) implantation (1). There are some factors that predispose eyes to CME after uneventful cataract surgery, including uveitis, retinal vein occlusion, and diabetes mellitus, and also after complicated cataract surgery (2,3). CME tends to resolve spontaneously or with pharmacological treatment (6, 7, 8, 9, 10 and 11); however, if it remains chronic, a permanent loss of central vision can occur. Clinical improvement can occur in eyes with no apparent vitreous traction.

Vitrectomy has been reported to be effective in treating CME, and some pseudophakic eyes with chronic CME that is unresponsive to medical treatment will recover good vision after vitrectomy (12, 13, 14, 15, 16, 17 and 18). In this chapter, we discuss the rationales for vitrectomy to treat aphakic/pseudophakic CME and report the indications and effectiveness of recent surgical techniques in treating CME.

Inflammatory responses are activated to different degrees in eyes that have undergone intraocular surgery. Prostaglandins (PGs) are released postoperatively by a disruption of the blood-retinal barrier caused by inflammation, hypotony, vitreous traction, and other complications. The PGs are metabolic breakdown products of arachidonic acid, and they have been postulated to be causative of CME (19

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