In this study, 25 eyes of 25 patients (9 women and 16 men) were included. All patients were followed for at least 24 months (mean 47.0 ± 20.5; range 24–96 months) after the initial PPV. The mean age was 76.2 ± 9.3 (range, 48–89) years at the initial PPV. Eighteen eyes were phakic and 7 eyes were pseudo-phakic at the time of surgery. The subtypes of nAMD were PCV in 18 eyes, RAP in 2 eyes, and unclassified in 5 eyes. The reasons for performing PPV were SMH (8 eyes) and VH (17 eyes) associated with nAMD. The average duration of SMH was 9.3 ± 4.6 (range 4–17) days. The average duration of VH was 45.9 ± 40.0 (range, 13–142) days, with the exception of 4 eyes with unknown duration. The average greatest diameter of the SMH was 4.0 ± 1.6 (range 2.0-6.7) disc diameters. Thirteen eyes had previously been treated with photocoagulation (PC), photodynamic therapy (PDT) or intravitreal injection of anti-VEGF drugs. Baseline characteristics of the patients are listed in Table 1.
Table 1
Baseline characteristics of the patients
Characteristics | |
Number of patients/eyes | 25/25 |
Gender male/ female | 16/9 |
Average age (range) years | 76.2 ± 9.3 (48–89) |
Subtype of AMD | |
PCV /RAP/ unknown | 18/2/5 |
Reason of initial vitrectomy | |
SMH/VH | 8/17 |
AMD: age related macular degeneration PCV: polypoidal choroidal vasculopathy |
RAP: retinal angiomatous proliferation SMH: submacular hemorrhage |
VH: vitreous hemorrhage |
Of the 17 eyes with VH, SMH was also detected during vitrectomy in 5 eyes. Simultaneous with PPV, the following procedures were performed: PEA-IOL in 17 eyes, injection of tPA into subretinal space in 13 eyes (8 eyes with SMH only, 5 eyes with VH and SMH), intravitreal injection of anti-VEGF agents in 6 eyes (3 eyes with SMH only, one eye with VH and SMH, 2 eyes with VH only), and fluid-air exchange with tamponade in 12 eyes (air in 1 eye, SF6 in 9 eyes, and silicon oil in 2 eyes).
Additional treatments after initial PPV in the 25 eyes are shown in Fig. 1. After the initial PPV, 10 eyes received intravitreal injection of anti-VEGF agent. One eye underwent PDT and subsequently received anti-VEGF therapy. Four eyes underwent repeat PPV for postoperative macular hole, postoperative proliferative vitreoretinopathy, silicon oil removal, and recurrent VH (1 eye each), 2 of which later received anti-VEGF therapy. Two eyes underwent PC. Eight eyes received no additional treatment. In the patient with recurrent VH after the initial PPV, retinal detachment occurred after the second PPV, and the third PPV and scleral buckling were performed. Therefore, a total of 13 eyes were initiated intravitreal anti-VEGF therapy and 12 eyes did not receive intravitreal anti-VEGF therapy. Subsequent analyses were conducted to compare these two groups.
In all patients, the mean BCVA improved significantly at 1, 3, 6, 12, 18, 24 (P < 0.01) months after PPV, and at the final visit (P < 0.05) (Fig. 2).
Of the 13 eyes that were given intravitreal injection of anti-VEGF agents, 12 eyes received aflibercept (IVA) and 1 eye received ranibizumab (IVR). There were no significant differences in gender ratio, age, presence of polyps, and baseline BCVA between the eyes with and those without anti-VEGF therapy. Regarding the reason for the initial PPV (SMH or VH), 6 of 8 eyes (75.0%) with SMH detected before PPV compared with 7 of 17 eyes (41.2%) with VH were treated with anti-VEGF therapy after vitrectomy, and the rate was apparently higher in eyes with SMH although there was no significant difference.
The mean BCVA of 13 eyes with anti-VEGF therapy improved significantly at 1 (P < 0.05), 3, 6, 12 (P < 0.01), 18 and 24 (P < 0.05) months. In comparison, the mean BCVA of 12 eyes without anti-VEGF therapy
improved significantly at 1, 3 and 6 (P < 0.05) months only (Fig. 3).
Of the 13 eyes with anti-VEGF therapy, BCVA improved in 9 eyes (69.2%) and worsened in 1 eye (7.7%) for more than 3 lines (15 letters) on the EDTRS chart at 24 months after PPV. Among the 12 eyes without anti-VEGF therapy, BCVA improved in 7 eyes (58.3%) and worsened in 1 eye (8.3%). The causes of vision loss were chronic macular edema in one eye with anti-VEGF therapy and macular atrophy after massive subretinal hemorrhage in one eye without anti-VEGF therapy.
The average duration from the initial PPV to initiation of anti-VEGF therapy was 7.54 ± 9.9 (range 1–32) months. The cumulative percentage of anti-VEGF therapy initiation during follow-up is shown in Fig. 4. In the 13 patients who received anti-VEGF therapy, the cumulative percentage of initiation was 53.8% at 2 months after surgery and 84.6% at 10 months. Anti-VEGF therapy was given by an as-needed regimen in 8 eyes and by a TAE regimen in 5 eyes (2 eyes converted to as-needed regimen). The mean follow-up period from the initiation of anti-VEGF therapy was 32.7 ± 17.0 (range 0–63) months, and the average number of anti-VEGF drug injections until the final observation was 6.2 ± 3.9 (range, 1–13). Three eyes underwent PDT after PPV. In one eye, PDT was performed before the initiation of anti-VEGF therapy. In this eye, the exudative change was not resolved after PDT, and anti-VEGF therapy was started resulting in dry macula. In the other two eyes, dry macula was not obtained even after the initiation of anti-VEGF therapy, and PDT was performed which achieved dry macula in one eye, but not in the other.
Five of the 13 eyes (38.5%) that started anti-VEGF therapy after PPV and 12 of 25 eyes (48.0%) of eyes that did not receive postoperative anti-VEGF therapy maintained dry macula for more than 1 year after the last injection. Eventually, 17 of 25 eyes (68.0%) with or without anti-VEGF therapy achieved dry macula.