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BACKGROUND/OBJECTIVES: To investigate if the visual and anatomic response to the first dexamethasone implant (DEX) predicts the 12-month clinical outcome after shifting to fluocinolone acetonide (FAc) implant in patients with diabetic macular oedema (DMO). METHODS: Retrospective cohort study including pseudophakic patients with previously treated DMO, undergone one or more DEX injections before FAc. Functional and morphologic response to DEX was defined based on the best-corrected visual acuity (BCVA) and central macular thickness (CMT) changes after the first DEX, respectively. Steroid-response was defined as intraocular pressure (IOP) elevation ≥5 mmHg or IOP > 21 mmHg after any previous DEX exposure. Pairwise comparisons for BCVA, CMT, and IOP after FAc were performed with linear mixed models and a repeated-measure design. RESULTS: Forty-four eyes of 33 patients were included. Patients were shifted to FAc after a mean ± standard deviation of 4.6 ± 3.2 DEX injections. Overall, BCVA and CMT improved during the first 12 months after switching to FAc (p = 0.04 and p

Over the past decade, great strides have been made in the management of diabetic macular edema (DME). Therapeutic alternatives now include focal/grid laser photocoagulation, vitreo-retinal surgery, and intraocular injection of anti-angiogenic and steroid molecules. Intravitreal administration of steroids represents a fundamental alternative for recalcitrant and naive eyes with DME, especially in those cases when anti-vascular endothelial growth factor (VEGF) agents are contraindicated or a treatment regimen with fewer intravitreal injections is required. Currently, 3 intravitreal corticosteroid options for DME treatment are available: the dexamethasone delivery system, the fluocinolone acetonide insert, and off-label intravitreal triamcinolone acetonide. All 3 agents are associated with risk of cataract progression and intraocular pressure elevation, but they maintain a good safety profile. In patients who remain unresponsive to anti-VEGF therapy, are pseudophakic, at low risk for glaucoma, or who have significant cardiovascular risk, treatment with long-lasting intraocular steroids is suggested. There still remain many unanswered questions about intravitreal drugs, regarding dose, frequency, the correct regimen of each treatment, and the potential long-term side effects.

Dexamethasone intravitreal implant 0.7 mg (DEX 0.7) was approved for treatment of diabetic macular edema (DME) after demonstration of its efficacy and safety in the MEAD registration trials. We performed subgroup analysis of MEAD study results to evaluate the efficacy and safety of DEX 0.7 treatment in patients with previously treated DME. Three-year, randomized, sham-controlled phase 3 study in patients with DME, best-corrected visual acuity (BCVA) of 34–68 Early Treatment Diabetic Retinopathy Study letters (20/200–20/50 Snellen equivalent), and central retinal thickness (CRT) ≥300 μm measured by time-domain optical coherence tomography. Patients were randomized to 1 of 2 doses of DEX (0.7 mg or 0.35 mg), or to sham procedure, with retreatment no more than every 6 months. The primary endpoint was ≥15-letter gain in BCVA at study end. Average change in BCVA and CRT from baseline during the study (area-under-the-curve approach) and adverse events were also evaluated. The present subgroup analysis evaluated outcomes in patients randomized to DEX 0.7 (marketed dose) or sham based on prior treatment for DME at study entry. Baseline characteristics of previously treated DEX 0.7 (n = 247) and sham (n = 261) patients were similar. In the previously treated subgroup, mean number of treatments over 3 years was 4.1 for DEX 0.7 and 3.2 for sham, 21.5 % of DEX 0.7 patients versus 11.1 % of sham had ≥15-letter BCVA gain from baseline at study end (P = 0.002), mean average BCVA change from baseline was +3.2 letters with DEX 0.7 versus +1.5 letters with sham (P = 0.024), and mean average CRT change from baseline was −126.1 μm with DEX 0.7 versus −39.0 μm with sham (P

Item does not contain fulltext PURPOSE: To confirm the safety and compare the efficacy of intravitreal pegaptanib sodium 0.3 mg versus sham injections in subjects with diabetic macular edema (DME) involving the center of the macula associated with vision loss not due to ischemia. DESIGN: Randomized (1:1), sham-controlled, multicenter, parallel-group trial. PARTICIPANTS: Subjects with DME. INTERVENTION: Subjects received pegaptanib 0.3 mg or sham injections every 6 weeks in year 1 (total = 9 injections) and could receive focal/grid photocoagulation beginning at week 18. During year 2, subjects received injections as often as every 6 weeks per prespecified criteria. MAIN OUTCOME MEASURES: The primary efficacy endpoint was the proportion gaining >/= 10 letters of visual acuity (VA) from baseline to year 1. Safety was monitored throughout. RESULTS: In all, 260 (pegaptanib, n = 133; sham, n = 127) and 207 (pegaptanib, n = 107; sham, n = 100) subjects were included in years 1 and 2 intent-to-treat analyses, respectively. A total of 49 of the 133 (36.8%) subjects from the pegaptanib group and 25 of the 127 (19.7%) from the sham group experienced a VA improvement of >/= 10 letters at week 54 compared with baseline (odds ratio [OR], 2.38; 95% confidence interval, 1.32-4.30; P = 0.0047). For pegaptanib-treated subjects, change in mean VA from baseline by visit was superior (P

PURPOSE. The purpose of this study was to investigate the effects of the extension of collateral vessels on the outcomes of eyes affected by central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO). METHODS. The study was designed as a cross-sectional case series. Patients affected by CRVO and BRVO were progressively recruited, along with an age- and sex-matched control group of healthy subjects. Structural optical coherence tomography (OCT) and OCT angiography (OCTA; 4.5 × 4.5 mm and 9.0 × 9.0 mm acquisitions) were performed on all participants in order to assess the relationship between the presence of collateral vessels and final anatomical outcomes - central macular thickness (CMT), foveal avascular zone - and functional outcomes - best corrected visual acuity (BCVA). RESULTS. Fifty-six eyes affected by CRVO and 47 eyes affected by BRVO were included. Baseline LogMAR BCVA was 0.41 ± 0.33 LogMAR in CRVO, and 0.39 ± 0.25 LogMAR in BRVO (P < 0.01), improving to 0.20 ± 0.26 LogMAR in CRVO (P < 0.01), and 0.19 ± 0.22 LogMAR in BRVO (P < 0.01). Baseline CMT was 511 ± 214 μm in CRVO and 482 ± 178 μm in BRVO (P > 0.05), decreasing to 328 ± 105 μm (P < 0.01) and 321 ± 78 μm in CRVO and BRVO, respectively (P < 0.01). Collateral vessels were detected in 16 of 56 eyes (29%) in CRVO and in 47 of 47 eyes (100%) in BRVO. Their extension was correlated with worse anatomic and visual outcomes. Remarkably, no correlation was found with peripheral capillary nonperfusion and vessel density impairment. CONCLUSIONS. The present study demonstrates that collateral vessel extension is associated with worse anatomic and functional outcomes in patients affected by CRVO and BRVO.

Purpose: To investigate baseline characteristics of patients undergoing additional antivascular endothelial growth factor (VEGF) injections for residual or recurrent diabetic macular edema (DME) in the first year after 0.19-mg fluocinolone acetonide (FAc) implant. Design: Prospective cohort study. Methods: Ninety-four eyes of 66 patients received an FAc implant. Eyes with persistent or recurrent DME were managed with pro re nata anti-VEGF agents. Demographic data and medical history were collected at baseline. Best-corrected visual acuity and central macular thickness were measured every 2 months. The 3 outcomes explored were 1) the risk factors for administration of additional anti-VEGF agents, 2) the interval from FAc to first anti-VEGF injection; and 3) the number of anti-VEGF doses required to maintain regression of DME. Results: Eighteen eyes (19.1%) of 13 patients received 1.3 ± 0.6 anti-VEGF injections. These eyes had significantly thicker central macular thickness at baseline and over the entire follow-up period (P < .001); best-corrected visual acuity was similar at every time point to eyes that were not receiving extra DME treatments. Eyes without preexistent panretinal photocoagulation (PRP) had a higher risk to undergo supplemental treatments (hazard ratio 1.5 [95% confidence interval 1.1-2.5, P = .03). The interval between FAc implant and the first anti-VEGF had a significant linear positive relationship with the number of dexamethasone implants before FAc implant (P = .002, R2 = 0.47). No association was found between baseline factors and the number of injections given. Conclusion: Anti-VEGF agents are efficient treatment to maintain visual acuity in residual/recurrent DME after FAc. Patients with higher baseline central macular thickness and with no previous central macular thickness are more likely to require additional treatments to control DME.

Various imaging modalities are of significant utility in the screening, grading, treatment, and follow-up of the different stages of diabetic retinopathy (DR) and diabetic macular edema. Color stereographic photography, fluorescein angiography, and optical coherence tomography (OCT) have been the gold standard for DR imaging for years. Besides these tools, newer technologies are gaining validation and popularity, such as fundus autofluorescence and OCT angiography. Furthermore, widefield retinography and ultra-widefield retinography have been introduced for a more comprehensive evaluation of the medium-far and very-far retinal peripheries, which is crucial for the assessment of the diverse manifestations of the disease. The aim of this review is to illustrate the recent advancements of the imaging systems for diagnosing DR, with a focus on the newest and noninvasive diagnostic tools.

Purpose: To evaluate the effects of repeated intravitreal dexamethasone implant. Methods: We reviewed the charts of 12 patients with diabetic macular edema, who received at least 2 intravitreal Ozurdex (0.7 mg) on an "as needed" basis. Main outcome measures included changes in best-corrected visual acuity, central macular thickness, retreatment interval, and incidence of side effects. Results: A total of 15 eyes of 12 patients (6 men, 6 women; mean age 62 +/- 12 years) were included. Retreatment was judged necessary after mean of 7.8 +/- 4.1 months from the first Ozurdex (median, 6 months) (15 of 15 eyes), mean of 4.8 +/- 0.9 months from the second Ozurdex (median, 5 months) (7 of 15 eyes), mean of 5.3 +/- 1.5 months from the third Ozurdex (median, 5 months) (3 of 15 eyes), and mean of 5.6 +/- 2 months from the fourth Ozurdex (median, 5 months) (3 of 15 eyes). Mean baseline best-corrected visual acuity was 0.67 +/- 0.33 logMAR in the overall diabetic macular edema population; it significantly improved to 0.53 +/- 0.31 logMAR after mean of 40.9 +/- 18.2 days from the first Ozurdex (peaking efficacy) (P < 0.001), to 0.53 +/- 0.29 logMAR after mean of 34.4 +/- 9.0 days from the second Ozurdex (peaking efficacy) (P < 0.003), and stabilized to 0.62 +/- 0.26 logMAR after mean of 29.8 +/- 12.1 days from the third Ozurdex (peaking efficacy) (P = 0.05), to 0.5 +/- 0.26 logMAR after mean of 36.3 +/- 3.2 days from the fourth Ozurdex (peaking efficacy) (P = 0.2), and to 0.50 +/- 0.26 logMAR after mean of 37.0 +/- 2.6 days from the fifth Ozurdex (peaking efficacy) (P = 0.2). Mean baseline central macular thickness significantly decreased from 546 +/- 139 mu m to 292 +/- 43 mu m at 39.4 +/- 17.9 days from the first Ozurdex (peaking efficacy) (P < 0.001), to 297 +/- 47 mu m at 33 +/- 9.4 days from the second Ozurdex (peaking efficacy) (P < 0.001), to 293 +/- 22 mu m at 29.8 +/- 12.1 days from the third Ozurdex (peaking efficacy) (P = 0.01), and stabilized to 309 +/- 35 mu m at 36.3 +/- 3.2 days from the fourth Ozurdex (peaking efficacy) (P = 0.1), and to 295 +/- 7 mu m at 37.0 +/- 2.6 days from the fifth Ozurdex (peaking efficacy) (P = 0.1). No serious adverse events were observed; three eyes developed a transient intraocular pressure increase, and cataract was extracted in one eye. Conclusion: Repeated intravitreal Ozurdex on an "as needed" basis with a variable retreatment interval may produce long-term clinically meaningful benefits in the treatment of diabetic macular edema, without other significant side effects than expected after intraocular corticosteroid treatment. Purpose: To evaluate the effects of repeated intravitreal dexamethasone implant. Methods: We reviewed the charts of 12 patients with diabetic macular edema, who received at least 2 intravitreal Ozurdex (0.7 mg) on an "as needed" basis. Main outcome measures included changes in best-corrected visual acuity, central macular thickness, retreatment interval, and incidence of side effects. Results: A total of 15 eyes of 12 patients (6 men, 6 women; mean age 62 +/- 12 years) were included. Retreatment was judged necessary after mean of 7.8 +/- 4.1 months from the first Ozurdex (median, 6 months) (15 of 15 eyes), mean of 4.8 +/- 0.9 months from the second Ozurdex (median, 5 months) (7 of 15 eyes), mean of 5.3 +/- 1.5 months from the third Ozurdex (median, 5 months) (3 of 15 eyes), and mean of 5.6 +/- 2 months from the fourth Ozurdex (median, 5 months) (3 of 15 eyes). Mean baseline best-corrected visual acuity was 0.67 +/- 0.33 logMAR in the overall diabetic macular edema population; it significantly improved to 0.53 +/- 0.31 logMAR after mean of 40.9 +/- 18.2 days from the first Ozurdex (peaking efficacy) (P < 0.001), to 0.53 +/- 0.29 logMAR after mean of 34.4 +/- 9.0 days from the second Ozurdex (peaking efficacy) (P < 0.003), and stabilized to 0.62 +/- 0.26 logMAR after mean of 29.8 +/- 12.1 days from the third Ozurdex (peaking efficacy) (P = 0.05), to 0.5 +/- 0.26 logMAR after mean of 36.3 +/- 3.2 days from the fourth Ozurdex (peaking efficacy) (P = 0.2), and to 0.50 +/- 0.26 logMAR after mean of 37.0 +/- 2.6 days from the fifth Ozurdex (peaking efficacy) (P = 0.2). Mean baseline central macular thickness significantly decreased from 546 +/- 139 mu m to 292 +/- 43 mu m at 39.4 +/- 17.9 days from the first Ozurdex (peaking efficacy) (P < 0.001), to 297 +/- 47 mu m at 33 +/- 9.4 days from the second Ozurdex (peaking efficacy) (P < 0.001), to 293 +/- 22 mu m at 29.8 +/- 12.1 days from the third Ozurdex (peaking efficacy) (P = 0.01), and stabilized to 309 +/- 35 mu m at 36.3 +/- 3.2 days from the fourth Ozurdex (peaking efficacy) (P = 0.1), and to 295 +/- 7 mu m at 37.0 +/- 2.6 days from the fifth Ozurdex (peaking efficacy) (P = 0.1). No serious adverse events were observed; three eyes developed a transient intraocular pressure increase, and cataract was extracted in one eye. Conclusion: Repeated intravitreal Ozurdex on an "as needed" basis with a variable retreatment interval may produce long-term clinically meaningful benefits in the treatment of diabetic macular edema, without other significant side effects than expected after intraocular corticosteroid treatment.

Aims: To evaluate changes in macular morphology and function after repeated intravitreal dexamethasone implant (Ozurdex((R))) for macular edema (ME) due to retinal vein occlusion (RVO). Methods: Consecutive treatment-naive patients with ME secondary to RVO were treated with Ozurdex and followed up to 12 months to evaluate functional and morphological outcomes by means of best-corrected visual acuity (BCVA) and microperimetry and by enhanced depth imaging optical coherence tomography, respectively. Results: Thirty-five eyes of 35 patients were included for the analysis (26 central RVO, 9 branch RVO). During the 12-month study period, 8 of the 35 eyes (23%) underwent 1 intravitreal dexamethasone implant, 13 of the 35 eyes (37%) underwent 2, and 14 of the 35 eyes (40%) underwent 3 intravitreal dexamethasone implants. At 1 month from the 1st intravitreal dexamethasone implant, the mean BCVA, retinal sensitivity and central macular thickness (CMT) significantly improved compared to the baseline values. At 3 months, the mean BCVA improvement was no more significant, while retinal sensitivity further improved and CMT slightly worsened, remaining, however, significantly better than at baseline. At 12 months, those eyes that had undergone 2 retreatments showed a significant improvement of the mean BCVA, mean retinal sensitivity and CMT compared to the baseline values [0.61 +/- 0.29 logarithm of the minimum angle of resolution (LogMAR) vs. 0.82 +/- 0.33 LogMAR, p = 0.011; 12.94 +/- 4.73 dB vs. 10.75 +/- 3.27 dB, p = 0.043, and 321 +/- 91 mu m vs. 735 +/- 169 mu m, p = 0.001, respectively]. In those eyes that had undergone only 1 retreatment, a significant improvement was recorded only for the CMT (500 +/- 224 mu m vs. 695 +/- 302 mu m, p = 0.044). The mean retreatment interval between the 1st and the 2nd injection was 4.5 +/- 1.1 months (range 3-7 months), and between the 2nd and the 3rd injection it was 4.1 +/- 1 months (range 3-6 months). Conclusions: In eyes with ME secondary to RVO, Ozurdex produces functional benefits as early as 1 month after treatment/retreatment. Current optical coherence tomography and microperimetry findings confirm the concept that, in most cases, the optimum retreatment interval should be

Purpose. To investigate changes in macular function after intravitreal dexamethasone implant (Ozurdex) for macular edema (ME) secondary to retinal vein occlusion (RVO). Methods. Nineteen treatment-naive patients with RVO-related ME were treated with intravitreal Ozurdex and followed up to 6 months to evaluate functional outcomes, by means of best-corrected visual acuity, microperimetry, and multifocal electroretinography, and their correlations with morphological parameters by enhanced depth imaging optical coherence tomography. Results. Nineteen eyes of 19 patients were included for analysis. At 1 month, mean best-corrected visual acuity, retinal sensitivity, and central macular thickness (CMT) improved from 0.50 +/- 0.34 LogMAR, 10.51 +/- 4.31 dB, and 762 +/- 259 mu m (baseline) to 0.38 +/- 0.34 LogMAR (p = 0.043), 12.28 +/- 5.06 dB (p = 0.025), and 385 +/- 191 mu m (p = 0.001), respectively. At 3 months, improvement of mean retinal sensitivity and CMT was still significant (11.62 +/- 5.05 dB [p = 0.047] and 518 +/- 251 mu m [p = 0.006]). Multifocal electroretinography measurements also showed (nonsignificant) improvement. No significant changes in choroidal thickness were recorded. Improvements recorded during the first 3 months were no longer significant from month 4. At each time point, we found a negative significant correlation between CMT and retinal sensitivity. Interestingly, 7 eyes did not undergo retreatment of less than 6 months; these eyes showed a significantly better baseline retinal sensitivity than eyes requiring retreatment of less than 6 months (12.27 +/- 3.52 dB vs. 9.48 +/- 4.53 dB [p = 0.038]). Conclusions. In eyes with ME secondary to RVO, intravitreal dexamethasone implant provides functional benefits as soon as 1 month after treatment. In most cases, the optimum retreatment interval is less than 6 months from first intravitreal Ozurdex. Microperimetry is a very useful tool to characterize macular function. Baseline macular sensitivity may predict the need for early (

Purpose: To study retinal function in asymptomatic Type 1 and Type 2 diabetic patients with nonproliferative diabetic retinopathy (NPDR) and no clinical signs of diabetic macular edema. Methods: Thirty-six consecutive Type 1 and Type 2 diabetic patients with nonproliferative diabetic retinopathy and no diabetic macular edema and 28 healthy controls underwent a complete ophthalmologic examination, including spectral domain optical coherence tomography and microperimetry. Results: Seventy-one eyes (17 patients with Type 1 and 19 with Type 2 diabetes) were tested, and data from 36 (17 Type 1 and 19 Type 2) eyes were analyzed. Mean best-corrected visual acuity was 0.00 +/- 0.01 logMAR and 0.00 +/- 0.02 logMAR for Type 1 and Type 2 diabetic patients, respectively (P = 0.075). Mean central foveal thickness was 234.5 +/- 13.7 mm and 256.3 +/- 12.7 mm for Type 1 and Type 2 diabetic patients, respectively (P = 0.04); the central foveal thickness was statistically different compared with the control groups (P = 0.04 and P = 0.01, respectively). Mean retinal sensitivity was 18.9 +/- 0.5 dB and 17.7 +/- 0.4 dB for Type 1 and Type 2 diabetic patients, respectively; it was statistically different compared with control groups (P < 0.0001 and P < 0.0001, respectively). Conclusion: We demonstrated a significantly reduced sensitivity in both nonproliferative diabetic retinopathy groups without diabetic macular edema compared with healthy controls; this reduction was greater in Type 2 diabetic patients. Central foveal thickness was increased in all diabetic patients compared with healthy controls, despite the absence of diabetic macular edema. Purpose: To study retinal function in asymptomatic Type 1 and Type 2 diabetic patients with nonproliferative diabetic retinopathy (NPDR) and no clinical signs of diabetic macular edema. Methods: Thirty-six consecutive Type 1 and Type 2 diabetic patients with nonproliferative diabetic retinopathy and no diabetic macular edema and 28 healthy controls underwent a complete ophthalmologic examination, including spectral domain optical coherence tomography and microperimetry. Results: Seventy-one eyes (17 patients with Type 1 and 19 with Type 2 diabetes) were tested, and data from 36 (17 Type 1 and 19 Type 2) eyes were analyzed. Mean best-corrected visual acuity was 0.00 +/- 0.01 logMAR and 0.00 +/- 0.02 logMAR for Type 1 and Type 2 diabetic patients, respectively (P = 0.075). Mean central foveal thickness was 234.5 +/- 13.7 mm and 256.3 +/- 12.7 mm for Type 1 and Type 2 diabetic patients, respectively (P = 0.04); the central foveal thickness was statistically different compared with the control groups (P = 0.04 and P = 0.01, respectively). Mean retinal sensitivity was 18.9 +/- 0.5 dB and 17.7 +/- 0.4 dB for Type 1 and Type 2 diabetic patients, respectively; it was statistically different compared with control groups (P < 0.0001 and P < 0.0001, respectively). Conclusion: We demonstrated a significantly reduced sensitivity in both nonproliferative diabetic retinopathy groups without diabetic macular edema compared with healthy controls; this reduction was greater in Type 2 diabetic patients. Central foveal thickness was increased in all diabetic patients compared with healthy controls, despite the absence of diabetic macular edema.

Purpose: To investigate the impact of intravitreal dexamethasone implant (Ozurdex) on macular morphology and function in eyes with macular edema secondary to central retinal vein occlusion. Methods: Twelve treatment-naive patients with decreased visual acuity because of central retinal vein occlusion-related macular edema were enrolled in this prospective uncontrolled study. Patients were treated with intravitreal Ozurdex and followed up at 1 month and 3 months for the evaluation of morphologic and functional outcomes, by means of best-corrected visual acuity, microperimetry, multifocal electroretinography, and customized high-resolution enhanced depth imaging spectral-domain optical coherence tomography scans. Results: Twelve eyes of 12 patients (10 men, 2 women; mean age 56.2 +/- 13.0 years) were included for analysis. At 1 month, mean best-corrected visual acuity, retinal sensitivity (microperimetry), multifocal electroretinography parameters, central macular thickness, and specific neurosensorial retinal measurements improved significantly. We found a significant negative correlation between retinal sensitivity and central macular thickness at 1 month and 3 months (r = -0.831, P = 0.001; r = -0.881, P = 0.001; respectively). Moreover, retinal sensitivity was negatively related to both outer and inner retinal thickness in all four intervals from the fovea. From baseline to Month 1, change in outer retinal thickness was positively related to multifocal electroretinography N1R1 amplitude change (r = 0.698, P = 0.012), whereas change in central macular thickness was negatively related to multifocal electroretinography P1R1 amplitude change (r = -0.701, P = 0.011). At 3 months, improvement of mean retinal sensitivity and central macular thickness slightly decreased. Conclusion: In eyes with macular edema secondary to central retinal vein occlusion, intravitreal dexamethasone provides functional benefits that correlate well with ultrastructural macular changes. Purpose: To investigate the impact of intravitreal dexamethasone implant (Ozurdex) on macular morphology and function in eyes with macular edema secondary to central retinal vein occlusion. Methods: Twelve treatment-naive patients with decreased visual acuity because of central retinal vein occlusion-related macular edema were enrolled in this prospective uncontrolled study. Patients were treated with intravitreal Ozurdex and followed up at 1 month and 3 months for the evaluation of morphologic and functional outcomes, by means of best-corrected visual acuity, microperimetry, multifocal electroretinography, and customized high-resolution enhanced depth imaging spectral-domain optical coherence tomography scans. Results: Twelve eyes of 12 patients (10 men, 2 women; mean age 56.2 +/- 13.0 years) were included for analysis. At 1 month, mean best-corrected visual acuity, retinal sensitivity (microperimetry), multifocal electroretinography parameters, central macular thickness, and specific neurosensorial retinal measurements improved significantly. We found a significant negative correlation between retinal sensitivity and central macular thickness at 1 month and 3 months (r = -0.831, P = 0.001; r = -0.881, P = 0.001; respectively). Moreover, retinal sensitivity was negatively related to both outer and inner retinal thickness in all four intervals from the fovea. From baseline to Month 1, change in outer retinal thickness was positively related to multifocal electroretinography N1R1 amplitude change (r = 0.698, P = 0.012), whereas change in central macular thickness was negatively related to multifocal electroretinography P1R1 amplitude change (r = -0.701, P = 0.011). At 3 months, improvement of mean retinal sensitivity and central macular thickness slightly decreased. Conclusion: In eyes with macular edema secondary to central retinal vein occlusion, intravitreal dexamethasone provides functional benefits that correlate well with ultrastructural macular changes.

Purpose: To evaluate the effects of repeated intravitreal dexamethasone implant (IDI) (Ozurdex (R)) in eyes with macular edema (ME) due to retinal vein occlusion (RVO). Methods: We reviewed the charts of patients with RVO-related ME, who received repeated Ozurdex IDI (0.7 mg) on an 'as-needed' basis. Main outcome measures included changes in best-corrected visual acuity (BCVA), central macular thickness (CMT), retreatment interval, and incidence of side effects. Results: A total of 33 eyes were included for analysis. Retreatment with Ozurdex was judged necessary after 4.7 +/- 1.1 months from the first IDI (1st IDI) and 5.1 +/- 1.5 months from the second IDI (2nd IDI). Baseline BCVA was 0.65 +/- 0.43 logMAR; it significantly improved to 0.50 +/- 0.42 logMAR after 1.4 +/- 0.7 months from the 1st IDI (peaking efficacy) (p < 0.001) and to 0.48 +/- 0.44 logMAR after 1.8 +/- 0.8 months from the 2nd IDI (peaking efficacy) (p < 0.001). CMT decreased from 636 +/- 217 mu m (baseline) to 300 +/- 114 mu m, 1.4 +/- 0.7 months after the 1st IDI (p < 0.001), and to 298 +/- 91 mu m, 1.8 +/- 0.8 months after the 2nd IDI (p < 0.001). A rebound effect was recorded in 7 eyes after the 1st IDI (mean 168 +/- 158 mu m) and in 4 eyes after the 2nd IDI (mean 215 +/- 199 mu m). All eyes with a rebound effect improved again after a 2nd intravitreal Ozurdex injection. No serious adverse events were observed; 12 eyes developed a transient IOP increase, and cataracts were extracted in 2 eyes. Conclusion: Repeated intravitreal Ozurdex on an 'as-needed' basis, with a retreatment interval

Purpose: To evaluate the effects of a single injection of Ozurdex over 6 months in eyes with persistent diabetic macular edema (DME). Methods: In this retrospective interventional study, 9 patients with decreased visual acuity, as a result of persistent DME, received Ozurdex (intravitreal dexamethasone implant 0.7 mg). Main outcome measures included changes in best-corrected visual acuity (BCVA) and central retinal thickness (CRT). Results: Nine eyes of 9 patients (5 males, 4 females; mean age 58 years) were included in the analysis. The mean duration of DME was 49.9 months (range 24-85). All patients had undergone previous treatments for DME (intravitreal injection of anti-vascular endothelial growth factor, steroids or laser photocoagulation) before entering the study. At baseline, the mean BCVA was 0.74 +/- 0.33 logMAR, and the mean CRT was 502 +/- 222.16 mu m. The mean BCVA was unchanged on the third day (0.74 +/- 0.38 logMAR, p = 0.5), improved to 0.62 +/- 0.32 logMAR (p = 0.02), 0.59 +/- 0.26 logMAR (p = 0.02) and 0.63 8 0.38 logMAR (p = 0.6) after the first, third and fourth months, respectively, and decreased again to 0.73 +/- 0.35 logMAR (p = 0.4) at 6 months. The mean CRT improved to 397 +/- 115.31 mu m (p = 0.17), 271 +/- 99.97 mu m (p = 0.007), 325 +/- 133.05 mu m (p = 0.03) and 462 +/- 176.48 mu m (p = 0.36) on the third day and after 1, 3 and 4 months of follow-up and then increased again to 537 +/- 265.42 mu m (p = 0.33) at 6 months. Eight patients needed retreatments in the sixth month. One eye developed a transient intraocular pressure (IOP) increase 1 month after injection, which was successfully managed with topical IOP-lowering medication. Conclusion: In eyes with persistent DME, Ozurdex produces improvement in BCVA and CRT as soon as the first days after the injection. Such improvement is maintained until the fourth month. Copyright (C) 2012 S. Karger AG, Basel Purpose: To evaluate the effects of a single injection of Ozurdex over 6 months in eyes with persistent diabetic macular edema (DME). Methods: In this retrospective interventional study, 9 patients with decreased visual acuity, as a result of persistent DME, received Ozurdex (intravitreal dexamethasone implant 0.7 mg). Main outcome measures included changes in best-corrected visual acuity (BCVA) and central retinal thickness (CRT). Results: Nine eyes of 9 patients (5 males, 4 females; mean age 58 years) were included in the analysis. The mean duration of DME was 49.9 months (range 24-85). All patients had undergone previous treatments for DME (intravitreal injection of anti-vascular endothelial growth factor, steroids or laser photocoagulation) before entering the study. At baseline, the mean BCVA was 0.74 +/- 0.33 logMAR, and the mean CRT was 502 +/- 222.16 mu m. The mean BCVA was unchanged on the third day (0.74 +/- 0.38 logMAR, p = 0.5), improved to 0.62 +/- 0.32 logMAR (p = 0.02), 0.59 +/- 0.26 logMAR (p = 0.02) and 0.63 8 0.38 logMAR (p = 0.6) after the first, third and fourth months, respectively, and decreased again to 0.73 +/- 0.35 logMAR (p = 0.4) at 6 months. The mean CRT improved to 397 +/- 115.31 mu m (p = 0.17), 271 +/- 99.97 mu m (p = 0.007), 325 +/- 133.05 mu m (p = 0.03) and 462 +/- 176.48 mu m (p = 0.36) on the third day and after 1, 3 and 4 months of follow-up and then increased again to 537 +/- 265.42 mu m (p = 0.33) at 6 months. Eight patients needed retreatments in the sixth month. One eye developed a transient intraocular pressure (IOP) increase 1 month after injection, which was successfully managed with topical IOP-lowering medication. Conclusion: In eyes with persistent DME, Ozurdex produces improvement in BCVA and CRT as soon as the first days after the injection. Such improvement is maintained until the fourth month. Copyright (C) 2012 S. Karger AG, Basel

Diabetic macular edema (DME), defined as a retinal thickening involving or approaching the center of the macula, plays a major role in vision loss related to diabetic retinopathy. This article presents an in-depth analysis of therapeutic perspectives on DME by means of an approach based on combination therapy with steroids. Corticosteroid drugs have been demonstrated to both inhibit the expression of vascular endothelial growth factor (VEGF) and the VEGF gene, and to have antiinflammatory properties. A treatment algorithm is provided regarding the management of DME. While grid laser photocoagulation remains the first-line therapy for focal vasogenic DME, diffuse DME can be effectively treated by means of intravitreal injections of corticosteroids. Recalcitrant DME can also be managed beneficially with intravitreal steroids. The management of DME is complex, and often multiple treatment approaches are needed. Each form of DME should be properly classified and specifically treated. The combination treatment has still an important role in the combined treatment options for DME. Copyright (C) 2010 S. Karger AG, Basel

Purpose1) To compare macular thickness (MT) by optical coherence tomography (OCT) in diabetics and controls; 2) to assess the relationship between MT and stage of diabetic retinopathy (DR) and macular edema (ME); 3) to quantify MT changes after laser treatment for ME.MethodsOne-hundred and thirty-seven patients with diabetes mellitus (216 eyes) were admitted to the study and examined by stereo-color fundus photos, retinal fluorangiography and OCT. DR was classified as: 1) no DR (46 eyes: 21.3%); 2) background DR (66 eyes: 30.6%); 3) pre-proliferative DR (50 eyes: 23.1%); 4) proliferative DR (54 eyes: 25%). The study group was then divided into three ME groups: 1) no edema (65 eyes: 30.1%); 2) not clinically significant ME (no CSME) (45 eyes: 20.8%); 3) clinically significant macular edema (CSME) (106 eyes: 49.1%). Three-month follow-up tomograms were taken to evaluate eyes laser-treated only for ME. The control group consisted of 50 eyes of 50 non-diabetic, age- and sex-matched subjects.ResultsMT was 369.3±163.2 μm in diabetics and 161.9±12.9 μm in controls (p 3 months, MT before and after treatment was 468.2±83. 17 μm and 372.1±120.63 μm.ConclusionsMT was greater in diabetics than controls and tended to increase with DR and ME severity. OCT is a sensitive technique for detecting early diabetic macular abnormalities and quantifying their reduction after laser treatment.

PURPOSE. To investigate the changes in macular choroidal thickness in eyes with various stages of diabetic retinopathy, using enhanced depth imaging optical coherence tomography (EDI OCT). METHODS. Sixty-three consecutive diabetic patients-who presented without diabetic retinopathy (NDR); with diabetic retinopathy (nonproliferative diabetic retinopathy [NPDR]) and no clinically significant macular edema (CSME+); or with NDPR and clinically significant macular edema (CSME+)-underwent EDI OCT. Twenty-one age-and sex-matched healthy subjects (21 eyes) also underwent EDI OCT. RESULTS. A total of 63 eyes of 63 consecutive diabetic patients (26 female [41.2%]; mean age 65 +/- 9 years, range 48-83 years) were included in the analysis. Mean best-corrected visual acuity was 0.13 +/- 0.25 LogMAR (range 0-1). Mean CMT was 272.5 +/- 16.2 mu m in 21 NDR eyes, 294.5 +/- 23.5 mu m in 21 NPDR/CSME- eyes, and 385.6 +/- 75.1 mu m in 21 NPDR/CSME+ eyes. There was no difference in mean subfoveal choroidal thickness among each diabetic group (238.4 +/- 47.9 mu m [NDR], 207.0 +/- 55.9 mu m [NPDR/CSME-], 190.8 +/- 48.4 mu m [NPDR/CSME+]; P = 0.23). The mean subfoveal choroidal thickness was significantly reduced in each diabetic group compared with the control group (309.8 +/- 58.5 mu m, P < 0.001). CONCLUSIONS. In diabetic eyes, there is an overall thinning of the choroid on EDI OCT. A decreased choroidal thickness may lead to tissue hypoxia and consequently increase the level of VEGF, resulting in the breakdown of the blood-retinal barrier and development of macular edema. (Invest Ophthalmol Vis Sci. 2012; 53: 6017-6024) DOI: 10.1167/iovs.12-9692 PURPOSE. To investigate the changes in macular choroidal thickness in eyes with various stages of diabetic retinopathy, using enhanced depth imaging optical coherence tomography (EDI OCT). METHODS. Sixty-three consecutive diabetic patients-who presented without diabetic retinopathy (NDR); with diabetic retinopathy (nonproliferative diabetic retinopathy [NPDR]) and no clinically significant macular edema (CSME+); or with NDPR and clinically significant macular edema (CSME+)-underwent EDI OCT. Twenty-one age-and sex-matched healthy subjects (21 eyes) also underwent EDI OCT. RESULTS. A total of 63 eyes of 63 consecutive diabetic patients (26 female [41.2%]; mean age 65 +/- 9 years, range 48-83 years) were included in the analysis. Mean best-corrected visual acuity was 0.13 +/- 0.25 LogMAR (range 0-1). Mean CMT was 272.5 +/- 16.2 mu m in 21 NDR eyes, 294.5 +/- 23.5 mu m in 21 NPDR/CSME- eyes, and 385.6 +/- 75.1 mu m in 21 NPDR/CSME+ eyes. There was no difference in mean subfoveal choroidal thickness among each diabetic group (238.4 +/- 47.9 mu m [NDR], 207.0 +/- 55.9 mu m [NPDR/CSME-], 190.8 +/- 48.4 mu m [NPDR/CSME+]; P = 0.23). The mean subfoveal choroidal thickness was significantly reduced in each diabetic group compared with the control group (309.8 +/- 58.5 mu m, P < 0.001). CONCLUSIONS. In diabetic eyes, there is an overall thinning of the choroid on EDI OCT. A decreased choroidal thickness may lead to tissue hypoxia and consequently increase the level of VEGF, resulting in the breakdown of the blood-retinal barrier and development of macular edema. (Invest Ophthalmol Vis Sci. 2012; 53: 6017-6024) DOI: 10.1167/iovs.12-9692

Purpose:To investigate the vasomotor responses and diameter of retinal vessels in patients with macular edema secondary to retinal vein occlusion (RVO).Methods:A total of 18 eyes of 18 RVO patients were consecutively included and compared with age- and sex-matched controls. Participants underwent an examination with optical coherence tomography and dynamic and static retinal vessel analyses using the Dynamic Vessel Analyzer.Results:Dynamic vessel analysis in RVO showed mean maximum venous and arterial dilation of 2.22 1.23% and 1.87 +/- 1.41%, respectively, as compared with 5.05 +/- 2.75% (P = 0.001) and 3.95 +/- 1.44% (P = 0.0004), respectively, in controls. Static retinal vessel analysis in RVO revealed a mean arteriovenous ratio (AVR) of 0.74 +/- 0.09 versus 0.90 +/- 0.04 (P < 0.0001) in controls. Mean AVRs of occluded and nonoccluded quadrants in RVO were 0.71 +/- 0.13 and 0.85 +/- 0.19, respectively; in the corresponding quadrants of controls, mean AVRs were 0.90 +/- 0.19 (P < 0.0001) and 0.86 +/- 0.17 (P = 0.89), respectively. In branch RVO patients, mean AVRs of occluded versus nonoccluded quadrants were 0.70 +/- 0.06 and 0.90 +/- 0.22 (P = 0.002), respectively.Conclusion:In patients with macular edema secondary to RVO, dynamic vessel analysis showed an impairment of both venous and arterial motility and/or reactivity and static vessel analysis showed a reduced AVR indicating a general enlargement of the retinal venous network. Moreover, in branch RVO patients, static analysis demonstrated that retinal vessels could actually be uninvolved by the occlusive process in areas spared by disease. OI Corvi, Federico/0000-0002-2661-5500 Purpose:To investigate the vasomotor responses and diameter of retinal vessels in patients with macular edema secondary to retinal vein occlusion (RVO).Methods:A total of 18 eyes of 18 RVO patients were consecutively included and compared with age- and sex-matched controls. Participants underwent an examination with optical coherence tomography and dynamic and static retinal vessel analyses using the Dynamic Vessel Analyzer.Results:Dynamic vessel analysis in RVO showed mean maximum venous and arterial dilation of 2.22 1.23% and 1.87 +/- 1.41%, respectively, as compared with 5.05 +/- 2.75% (P = 0.001) and 3.95 +/- 1.44% (P = 0.0004), respectively, in controls. Static retinal vessel analysis in RVO revealed a mean arteriovenous ratio (AVR) of 0.74 +/- 0.09 versus 0.90 +/- 0.04 (P < 0.0001) in controls. Mean AVRs of occluded and nonoccluded quadrants in RVO were 0.71 +/- 0.13 and 0.85 +/- 0.19, respectively; in the corresponding quadrants of controls, mean AVRs were 0.90 +/- 0.19 (P < 0.0001) and 0.86 +/- 0.17 (P = 0.89), respectively. In branch RVO patients, mean AVRs of occluded versus nonoccluded quadrants were 0.70 +/- 0.06 and 0.90 +/- 0.22 (P = 0.002), respectively.Conclusion:In patients with macular edema secondary to RVO, dynamic vessel analysis showed an impairment of both venous and arterial motility and/or reactivity and static vessel analysis showed a reduced AVR indicating a general enlargement of the retinal venous network. Moreover, in branch RVO patients, static analysis demonstrated that retinal vessels could actually be uninvolved by the occlusive process in areas spared by disease.