Angiographic findings before and after the onset of brolucizumab-associated retinal vascular occlusion and intraocular inflammation.

PURPOSE

To describe angiographic features of a case of delayed-onset retinal vascular occlusion and intraocular inflammation (IOI) following brolucizumab intravitreal injection (IVI).

OBSERVATIONS

A 75-year-old woman with advanced age-related macular degeneration (AMD) complained of persistent distorted vision despite 1 aflibercept 2-mg IVI and subsequent 1 brolucizumab 6-mg IVI. At 20 days after brolucizumab IVI, clinical examination showed no signs of IOI, her right best-corrected visual acuity (BCVA) was 1.0 (Snellen equivalent, 20/20). Simultaneous fluorescein and indocyanine green angiography (FA/IA) performed 2 days later showed no abnormalities, but she noticed floaters and decreased vision in her right eye 5-6 hours after FA/IA. At 44 days after brolucizumab IVI, her right BCVA was 0.6 (Snellen equivalent, 20/33), and clinical examination revealed mutton-fat keratic precipitates, anterior chamber cells (2+), vitreous cells, vitreous haze (1+), and sheathed retinal vessels. FA showed filling defect and vascular staining/leakage at several retinal arteries and dye leakage from optic disc edge, where IA demonstrated dye staining as well. However, there was a retinal artery occlusion site which lacks angiographic signs indicative of active retinal vasculitis. The patient was diagnosed with retinal vascular occlusion and IOI which occurred approximately 3 weeks after brolucizumab IVI.

CONCLUSIONS AND IMPORTANCE

Delayed brolucizumab-associated retinal vascular occlusion and IOI can develop from a condition in which no apparent abnormal findings exist on FA/IA. Together with the fact that angiographic signs observed in this case were not severe enough to induce retinal artery occlusion, potent and prolonged vascular endothelial growth factor inhibition by brolucizumab IVI might have caused severe damage to retinal vascular endothelial cells. Then, the damage subsequently led to retinal vascular occlusions and enhanced immune reaction to brolucizumab. The latter would be enhanced through the migration of immune cells towards vitreous cavity being allowed by disrupted inner blood retinal barrier.