Incidence Of Clinical Cystoid Macular Edema Research Articles

Postsurgical Cystoid Macular Edema.

Cystoid macular edema (CME) is a primary cause of reduced vision following both cataract and successful vitreoretinal surgery. The incidence of clinical CME following modern cataract surgery is 0.1-2.35%. Preexisting conditions such as diabetes mellitus and uveitis as well as intraoperative complications can raise the risk of postsurgical CME. The etiology of CME is not completely understood. Prolapsed or incarcerated vitreous and postoperative inflammatory processes have been proposed as causative agents. Pseudophakic CME is characterized by poor postoperative visual acuity. Fluorescein angiography shows the classical perifoveal petaloid staining pattern and late leakage of the optic disk. Optical coherence tomography is a useful diagnostic tool, which displays cystic spaces in the outer nuclear layer. The most important differential diagnoses include age-related macular degeneration and other causes of CME such as diabetic macular edema. Most cases of pseudophakic CME resolve spontaneously. The value of prophylactic treatment is doubtful. First-line treatment of postsurgical CME should include topical nonsteroidal anti-inflammatory drugs and corticosteroids. Oral carbonic anhydrase inhibitors can be considered complementary. In cases of resistant CME, periocular or intraocular corticosteroids present an option. Antiangiogenic agents, though experimental, should be considered for nonresponsive persistent CME. Surgical options should be reserved for special indications.

Efficacy of topical flurbiprofen and indomethacin in preventing pseudophakic cystoid macular edema

We evaluated two topical cyclo-oxygenase inhibitors (COIs), 0.03% flurbiprofen and 1 % indomethacin, for their ability to prevent pseudophakic cystoid macular edema (CME). The study was a randomized, doublemasked, vehicle-controlled, parallel group, clinical trial for six months at eight sites in Canada and two in Germany. The study population consisted of 681 patients who had extracapsular cataract extraction and posterior chamber lens implantation. Flurbiprofen, indomethacin, or the vehicle was instilled into the eye four times daily for two days preoperatively and three months postoperatively. Results were measured by angiographic and clinical CME at visit 5 (day 21–60) and visit 7 (day 121–240) and by contrast sensitivity and Snellen visual acuity at all five postoperative visits. At visit 5, the incidence of angiographic CME was comparable in the two COI treatment groups (16.8% flurbiprofen, 12.4% indomethacin) and was significantly lower than in the vehicle group (32.2%). The incidence of clinical CME was also significantly lower in the COI-treated groups (10.7% flurbiprofen, 9.6% indomethacin) than in the vehicle group (21.9%). By visit 7, the incidence of angiographic CME had declined to between 4% and 8% and the incidence of clinical CME was less than 2% in all three groups. At visit 5, contrast sensitivity scores were significantly worse in vehicle-treated patients with angiographic CME than in those without CME, and Snellen visual acuity was one line worse in patients with CME. Flurbiprofen-treated patients achieved good Snellen visual acuity (better than 20/40) sooner than vehicle-treated patients. The results suggest that angiographic evidence of CME is related to a clinically relevant decrease in visual function and that treatment with flurbiprofen or indomethacin reduces the incidence and severity of CME and the associated visual dysfunction in the early postoperative period.