Aims: To identify incident macular atrophy and evaluate antecedent anatomic alterations in eyes with neovascular age-related macular degeneration (NVAMD) that were treated with anti-vascular endothelial growth factor (anti-VEGF) agents. Methods: All patients treated with anti-VEGF agents for NVAMD by one of the authors during the 2014 calendar year who had follow up ≥ 12 months had evaluation of all SD-OCT scans from first treatment (usually prior to 2014) to last follow up through June 2018. Results: The ascertainment procedure identified 342 eyes of 278 patients with NVAMD among which 47 developed macular atrophy. The median time from treatment initiation to development of macular atrophy was 29.6 (interquartile range, 17.7-43.4) months. Three macular alterations were identified in areas that developed atrophy (some eyes had more than one); collapse of a vascularized pigment epithelial detachment (PED) and regression of choroidal neovascularization (CNV) in 25 eyes, development of subretinal hyper-reflective material and/or subretinal fibrosis in 15 eyes, or atrophy occurring in association with large drusen and pigmentary changes resulting in an arc of atrophy in a pattern typically referred to as geographic atrophy in 13 eyes. Conclusions: These data suggest that in some instances CNV may compensate for choroidal ischemia and the loss of CNV may expose retinal pigmented epithelial cells and photoreceptors to ischemic damage and atrophy.

Aims: To identify incident macular atrophy and evaluate antecedent anatomic alterations in eyes with neovascular age-related macular degeneration (NVAMD) that were treated with anti-vascular endothelial growth factor (anti-VEGF) agents. Methods: All patients treated with anti-VEGF agents for NVAMD by one of the authors during the 2014 calendar year who had follow up ≥ 12 months had evaluation of all SD-OCT scans from first treatment (usually prior to 2014) to last follow up through June 2018. Results: The ascertainment procedure identified 342 eyes of 278 patients with NVAMD among which 47 developed macular atrophy. The median time from treatment initiation to development of macular atrophy was 29.6 (interquartile range, 17.7-43.4) months. Three macular alterations were identified in areas that developed atrophy (some eyes had more than one); collapse of a vascularized pigment epithelial detachment (PED) and regression of choroidal neovascularization (CNV) in 25 eyes, development of subretinal hyper-reflective material and/or subretinal fibrosis in 15 eyes, or atrophy occurring in association with large drusen and pigmentary changes resulting in an arc of atrophy in a pattern typically referred to as geographic atrophy in 13 eyes. Conclusions: These data suggest that in some instances CNV may compensate for choroidal ischemia and the loss of CNV may expose retinal pigmented epithelial cells and photoreceptors to ischemic damage and atrophy.

The choroid is a multifunctional, highly vascular, and dynamic tissue which contributes to ocular homeostasis and the regulation of eye growth in both animals and humans. Although challenging to reliably measure, recent advances in ocular imaging (particularly optical coherence tomography) has expanded the current understanding of the role of the choroid in ageing and refractive error development during childhood. This commentary considers recent advances in the field, particularly the impact of orthokeratology on choroidal thickness and contour in myopic children, and the potential use of choroidal metrics as a biomarker for future eye growth.

The choroid is a multifunctional, highly vascular, and dynamic tissue which contributes to ocular homeostasis and the regulation of eye growth in both animals and humans. Although challenging to reliably measure, recent advances in ocular imaging (particularly optical coherence tomography) has expanded the current understanding of the role of the choroid in ageing and refractive error development during childhood. This commentary considers recent advances in the field, particularly the impact of orthokeratology on choroidal thickness and contour in myopic children, and the potential use of choroidal metrics as a biomarker for future eye growth.

Aim: The objective of this study was to investigate the prognosis of massive vitreous hemorrhage(VH) secondary to polypoidal choroidal vasculopathy(PCV) after vitrectomy.  

Methods: Forty-nineeyes in 48 patients with PCV and breakthrough VH who underwent 23-gauge pars plana vitrectomy between January 2015 and December 2020 were enrolled. The main outcome parameters were best-corrected visual acuity, postoperative adverse events, and reoperation.

Results:The average follow-up time was 20.0±15.82 months. The average preoperative best-corrected visual acuity (BCVA) was 2.12±0.65 logarithm of the minimum angle of resolution (logMAR), the BCVA at six monthswas 1.65±0.64 logMAR, and the six-month follow-up BCVA was 1.67±0.76 logMAR. Compared to the average preoperative BCVA, the six-months and last follow-up BCVA after vitrectomy improved (P<0.05). The BCVAat the fnal follow-up was better than 1.3logMAR only in 14 eyes (28.6%). Postoperative complications were observed in 10 eyes (20.4%), including recurrent retinal detachment, recurrent vitreous hemorrhage, macular hole, hyphema and lens dislocation. Fourteen eyes(28.6%) underwent cataract surgery procedure an average of 10.16±5.14 months after vitrectomy. BCVAone week and three monthsafter cataract surgery improved compared toBCVAbefore cataract surgery (P<0.05). Hypertension was associated with BCVAsix months after vitrectomy (P=0.017). The BCVA at baseline and three months after PPV were worse in patients who underwent vitrectomy combined with silicone oil filling (P<0.05). Eyes with postoperative complications had worse BCVA at six months, 12 months, and at the final follow-up after PPV (P<0.05).The duration of VH is related to the BCVA12 months after PPV visual acuity after surgery. Patients who underwent vitrectomy within one month of the onset of vitreous hemorrhage had better BCVA 12 months after vitrectomy than those who underwent vitrectomy surgery one month later (P=0.015). 

Conclusions: Although the prognosis of vitrectomy varies greatly, cataract surgery could be considered to improve BCVAif polypoidal lesions are inactive six months after vitrectomy.

Aim: The objective of this study was to investigate the prognosis of massive vitreous hemorrhage(VH) secondary to polypoidal choroidal vasculopathy(PCV) after vitrectomy.

Methods: Forty-nineeyes in 48 patients with PCV and breakthrough VH who underwent 23-gauge pars plana vitrectomy between January 2015 and December 2020 were enrolled. The main outcome parameters were best-corrected visual acuity, postoperative adverse events, and reoperation.

Results:The average follow-up time was 20.0±15.82 months. The average preoperative best-corrected visual acuity (BCVA) was 2.12±0.65 logarithm of the minimum angle of resolution (logMAR), the BCVA at six monthswas 1.65±0.64 logMAR, and the six-month follow-up BCVA was 1.67±0.76 logMAR. Compared to the average preoperative BCVA, the six-months and last follow-up BCVA after vitrectomy improved (P<0.05). The BCVAat the fnal follow-up was better than 1.3logMAR only in 14 eyes (28.6%). Postoperative complications were observed in 10 eyes (20.4%), including recurrent retinal detachment, recurrent vitreous hemorrhage, macular hole, hyphema and lens dislocation. Fourteen eyes(28.6%) underwent cataract surgery procedure an average of 10.16±5.14 months after vitrectomy. BCVAone week and three monthsafter cataract surgery improved compared toBCVAbefore cataract surgery (P<0.05). Hypertension was associated with BCVAsix months after vitrectomy (P=0.017). The BCVA at baseline and three months after PPV were worse in patients who underwent vitrectomy combined with silicone oil filling (P<0.05). Eyes with postoperative complications had worse BCVA at six months, 12 months, and at the final follow-up after PPV (P<0.05).The duration of VH is related to the BCVA12 months after PPV visual acuity after surgery. Patients who underwent vitrectomy within one month of the onset of vitreous hemorrhage had better BCVA 12 months after vitrectomy than those who underwent vitrectomy surgery one month later (P=0.015). 

Conclusions: Although the prognosis of vitrectomy varies greatly, cataract surgery could be considered to improve BCVAif polypoidal lesions are inactive six months after vitrectomy.