cystoid macular edema (CME) is a painless disease with different etiologies, which manifests as multiple cyst like (cystoid) spaces in the macula. CME is a common cause of vision loss following cataract surgery. Some risk factors for post-cataract surgery CME include intraoperative complications specially incarceration of vitreous in the surgical wound, history of diabetes, uveitis and postoperative inflammation and infection. Clinical examination, fluorescein angiography and OCT are beneficial in the diagnosis of this disease. Since, it is a self-limiting disease, no standard therapy has been developed despite topical NSAIDs, periocular and intravitreal steroid injection and oral carbonic anhydrase inhibitors are used in chronic cases.

Purpose: To review methods of diagnosis and treatment of cystoid macular edema after cataract surgery. Materials and Methods: We searched all papers up to 2000 regarding the key words: cystoid macular edema, diagnosis, and treatment at the Medline. We reviewed the relevant articles and compared the results and discussed about them according our own experiences. Results and discussion: cystoid macular edema should be considered in the evaluation of loss of vision after cataract surgery in any patient. There are several methods for diagnosing the cystoid macular edema, but the most important one is funduscopy. Although new techniques like optical cohererce tomography and infrared scanning laser ophthalmoscopy can exactly determine the thickness of retina, they are not widely used and they are very expensive instruments. Therefor the best way for diagnosis of cystoid macular edema is physical examination and fluorescein angiography. The most controversies are around treatment of cystoid macular edema. The first step is treating the existing complications during the surgery, especially vitreous or iris adhesion to the wound. Postoperative inflammation should be treated by administration of corticosteroids and /or cyclooxygenase inhibitors. Even in the absence of inflammation and in the chronic cases, administration of cyclooxygenase inhibitors improves cystoid macular edema, but recurrences are frequent. Cyclooxygenase inhibitors are also widely used for prevention of cystoid macular edema. In the chronic nonresponsive cases with considerable loss of vision, vitrectomy is indicated. Conclusion: The major known cause of cystoid macular edema is prostaglandin production and so tbe most effective way for prevention is breaking this process by using cyclooxygenase inbibitors. In the presence of complication, corticosteroids should be administered. In the chronic nonresponsive cases, even in the absence of other complications, vitrectomy is highly recommended.

cystoid macular edema (CME) is a major cause of decreased vision after complicated or uncomplicated cataract surgery. This paper reviews the use of intravitreal bevacizumab (IVB) injection for treatment of pseudophakic CME. In a literature search of all articles available on Medline and Scopus databases, 11 studies including one prospective and 4 retrospective studies, 4 case reports, one letter to editor and one review article were identified. All articles except one, reported the use of IVB for chronic CME unresponsive to at least one conventional treatment modality. The level of evidence for all studies was categorized as low or very low. Although intravitreal bevacizumab might be effective for many cases of pseudophakic CME, its use should be reserved for eyes unresponsive to conventional treatment modalities.

cystoid macular edema is rarely observed secondary to paclitaxel treatment. A 55-year-old female patient was applied five cures of paclitaxel and carboplatin chemotherapy after being diagnosed with metastatic ovarian cancer. The patient had a normal bilateral vision prior to the chemotherapy treatments. After the fifth cure, the patient complained of bilateral vision loss, which was more severe in the left eye. Ophthalmologic examination revealed that right eye vision was 4/10 blurred without glasses and 7/10 blurred with glasses, left eye vision was 1/10 blurred without glasses and 4/10 blurred with glasses. Pathology was not detected during the biomicroscopic examination. Fundus examination of the patient revealed pigment epithelium irregularity, which was found to be less in the right eye, and it was found a decrease in foveal cavity. For fundus examination, the patient underwent fundus fluorescein angiography (FFA) and optical coherence tomography (OCT). FFA revealed fluorescein leakage and cystoid appearance particularly more apparent in the left eye. Thickening in the macula and cystoid space was observed particularly more in the left eye in the OCT measurement. In conclusion, we presented our case as a rarely observed cystoid macular edema secondary to paclitaxel treatment.

Background: cystoid macular edema (CME) is the leading cause of permanent visual impairment in patients with uveitis, particularly in patients with intermediate uveitis (IU). This study was aimed at comparing the changes in the macular microvasculature in patients with IU with uveitic non-responsive CME and without macular edema. Methods: In this case-control study, 55 eyes of patients with IU were assessed for macular microvascular structures, including vascular density, foveal avascular zone (FAZ) measurement, and vascular morphological changes, using spectral-domain optical coherence tomography angiography (OCT-A) with the AngioVue OCT-A system. We divided patients into the following two groups: the case group, including 30 eyes with IU-related non-responsive CME, and the control group, including 25 eyes with IU without macular edema. Results: Participants in the case and control groups had comparable age (P = 0. 753) and sex (P = 0. 124) distributions. Superficial capillary plexus vessel density in the case group was significantly decreased in the whole image (P = 0. 027) and the parafoveal area (P = 0. 001) compared to the control group. However, there were no statistically significant differences between the two groups in terms of foveal superficial vessel density, deep capillary plexus vessel density, FAZ area, FAZ perimeter, FAZ acircularity index, or foveal vessel density in a 300-µ, m-wide annulus around the FAZ (all P > 0. 05). Vascular morphological changes, such as the capillary tuft, telangiectatic vessels, or micro-aneurism, were not different in the overview images of the OCT-A printout between the two groups. Conclusions: The mean superficial capillary plexus vessel density was lower in eyes with IU-related nonresponsive CME than in those without macular edema. We observed more cystoid spaces in SCP than in DCP. Microcystic changes in the inner retina and ischemia may be the underlying cause in eyes with nonresponsive CME. Future prospective longitudinal studies with healthy, matched controls are warranted to confirm our findings.

Lipofuscin results from digestion of photoreceptor outer segments by the retinal pigment epithelium (RPE) and is the principal compound that causes RPE fluorescence during autofluorescence imaging. Absorption of the 488-nanometer blue light by macular pigments, especially by the carotenoids lutein and zeaxanthin, causes normal macular hypo-autofluorescence. Fundus autofluorescence imaging is being increasingly employed in ophthalmic practice to diagnose and monitor patients with a variety of retinal disorders. In macular edema for example, areas of hyper-autofluorescence are usually present which are postulated to be due to dispersion of macular pigments by pockets of intraretinal fluid. For this reason, the masking effect of macular pigments is reduced and the natural autofluorescence of lipofuscin can be observed without interference. In cystic types of macular edema, e.g. cystoid macular edema due to retinal vein occlusion, diabetic macular edema and post cataract surgery, hyperautofluorescent regions corresponding to cystic spaces of fluid accumulation can be identified. In addition, the amount of hyper-autofluorescence seems to correspond to the severity of edema. Hence, autofluorescence imaging, as a noninvasive technique, can provide valuable information on cystoid macular edema in terms of diagnosis, followup and efficacy of treatment.

Purpose: To assess the effectiveness of intravitreal injection of triamcinolone acetonide on macular edema associated with branch retinal vein occlusion (BRVO).Design: A prospective noncomparative interventional case series.Patients & Methods: Fourteen eyes of 14 patients with macular edema associated with BRVO were enrolled. In all patients after thorough ophthalmic examination, 4 mg triamcinolone acetonide was injected intravitreally then all eyes followed at 1 day, 1 week, 1, 3 and 6 months. Ten eyes were followed until 9 months. Central macular thickness was measured with Optical Coherence Tomography (OCT) at baseline and 3 months after injection. Best Corrected Visual Acuity (BCVA) and 1-mm central macular thickness were main outcome measurements.Results: Mean baseline BCVA: 1.33±0.52: logarithm of Minimum Angle of Resolution (logMAR) improved to 0.81±0.56 (P=0.002) at 1 month, 0.65±0.48 (P=0.001) at 3 months, but decreased to 0.85±0.44 (P=0.005) at 6 months. In 10 eyes of 14 eyes that were followed for 9 months, mean BCVA decreased to 1.20±0.48 (P=0.171). A 32% reduction of pre injection value of 1 mm central foveal thickness observed at 3 months (565±199.58 mm versus 383.78±145.70 mm, P=0.001). Ocular hypertension was developed in six patients that were controlled by topical antiglaucoma medication. Cataract developed or progressed in two eyes.Conclusion: Intravitreal triamcinolone acetonide can decrease macular edema and improve visual acuity in BRVO in short term but further study is required with control group and longer follow up to clarify the benefits and risks of this treatment.