Prognostic Factors in Patients with Persistent Full-Thickness Idiopathic Macular Holes Treated with Re-Vitrectomy with Autologous Platelet Concentrate.

PURPOSE: To identify the predictors for anatomical and functional outcome after re-vitrectomy with application of autologous platelet concentrate (APC) in eyes with persistent idiopathic macular hole (MH). METHODS: Retrospective study of 103 eyes with persistent MHs after vitrectomy with peeling of internal limiting membrane (ILM) and expansive gas. All patients underwent re-vitrectomy with APC and endotamponade. The anatomical MH closure rate and postoperative best-corrected visual acuity (BCVA) were evaluated. Further, predictive factors influencing the success of the surgery were analyzed. RESULTS: Median BCVA (logMAR) before the surgery was 1.00 (interquartile range [IQR] 0.80-1.30) and the median of minimum diameter between hole edges was 508 µm (IQR 387-631). The final closure rate after re-vitrectomy with APC was 60.2% (62 of 103 eyes). The following predictors were identified to significantly influence the closure rate: tractional hole index (THI), axial length, time between first and second surgery, and the experience of the surgeon (p < 0.05). CONCLUSIONS: Re-vitrectomy with APC led to the closure of 60.2% of the persistent MHs. The closure rate negatively correlates with increasing axial length, time between the first and second surgery, and the decreased THI. Further, experienced surgeons (with a history of >100 pars plana vitrectomies with ILM peeling) had significantly higher closure rates.

Baseline predictors for visual acuity loss during observation in diabetic macular oedema with good baseline visual acuity.

PURPOSE: To investigate clinical baseline characteristics and optical coherence tomography biomarkers predicting visual loss during observation in eyes with diabetic macular oedema (DMO) and good baseline visual acuity (VA). METHODS: A sub-analysis of a 12-month, retrospective study, including patients with baseline VA ≤0.1 logMAR (≥20/25 Snellen) and centre-involving DMO. The primary outcome measure was the correlation between baseline characteristics and VA loss ≥10 letters during follow-up. RESULTS: A total of 249 eyes were included in the initial study, of which 147 eyes were observed and 80 eyes received anti-vascular endothelial growth factor (VEGF) treatment at baseline. Visual acuity (VA) loss ≥10 letters occurred in 21.8% (observed cohort) and in 24.3% (treated cohort), respectively. Within observed eyes, presence of hyperreflective foci [HRF; odds ratio (OR): 3.18, p = 0.046], and disorganization of inner retina layers (DRIL; OR: 2.71, p = 0.026) were associated with a higher risk of VA loss ≥10 letters. In observed eyes with a combined presence of HRF, DRIL and ellipsoid zone (EZ) disruption, the risk of VA loss was further increased (OR: 3.86, p = 0.034). In eyes with combined presence of DRIL, HRF and EZ disruption, risk of VA loss was 46.7% (7/15 eyes) in the observed cohort, and 26.3% (5/19 eyes) in the treated cohort (p = 0.26). CONCLUSION: Patients with DMO and good baseline VA, managed by observation, are of increased risk for VA loss if DRIL, HRF and EZ disruption are present at baseline. Earlier treatment with anti-VEGF in these patients may potentially decrease the risk of VA loss at 12 months.

Real-world outcomes of non-responding diabetic macular edema treated with continued anti-VEGF therapy versus early switch to dexamethasone implant: 2-year results.

AIMS: To provide 2-year follow-up data on eyes with diabetic macular edema (DME) that were non-responsive after three initial anti-vascular endothelial growth factor (VEGF) injections, comparing functional and anatomical outcomes under continued anti-VEGF therapy versus dexamethasone (DEX) implant. METHODS: Multicenter, retrospective chart review comparing eyes with treatment-naïve DME and a suboptimal response to a loading phase of anti-VEGF therapy (3 injections given monthly) which were then treated with (a) further anti-VEGF (n = 72) or (b) initially switched to DEX implant (n = 38). Main outcome measures were change in visual acuity (VA) and central subfield thickness (CST) from the end of the loading phase to 24 months. RESULTS: In 79% of the 12-month study population (87/110 eyes), 24-month data were available. One quarter of eyes in each group switched treatments during the second year. Eyes that were switched early to DEX implant maintained the functional and anatomical improvements at 24 months which were seen in the first year (from month 3: + 8.9 letters, - 214 µm). Eyes that were switched from anti-VEGF therapy to steroids in the second year improved VA and reduced CST at 24 months (from month 12: + 6.8 letters, p = 0.023; - 226 µm, p = 0.004). In eyes continued on anti-VEGF therapy, VA and CST were stable at 24 months (from month 3: + 2.8 letters, p = 0.254; - 24 µm, p = 0.243). Eyes that were non-responsive to anti-VEGF therapy for 12 months had similar chances to experience a VA gain from further therapy as eyes that were non-responsive for 3 months only (23.8 vs. 31.0%, p = 0.344). CONCLUSIONS: The beneficial effect of an early switch to DEX implant in DME non-responders seen at month 12 was maintained during the second year. A later switch from anti-VEGF to steroids still provided significant improvement. Eyes continued on anti-VEGF over a period of 24 months maintained vision. A quarter of eyes, which had not improved vision at 12 months, exhibited a delayed response to treatment.