Exploring the Relation Between Peripapillary Retinal Vessel Caliber and Visual Field Defects in Primary Open-Angle Glaucoma

Abstract

Background Primary open-angle glaucoma (POAG) is a progressive optic neuropathy characterized by loss of retinal ganglion cells, optic nerve head changes, and visual field defects. Vascular factors, alongside intraocular pressure, play a crucial role in POAG pathogenesis, and this study aims to explore the relationship between retinal vessel caliber and visual field defects in POAG patients. Purpose To evaluate the association between retinal vessel calibers in the peripapillary area with visual field defects in one or both hemifields. Materials and Methods This cross-sectional study was conducted at a tertiary eye care center in northern Karnataka for one year, enrolling 100 eyes from 50 primary open-angle glaucoma (POAG) patients with visual field abnormalities. Fundus color stereoscopic photographs were taken using a Canon digital camera, and diameters of the superior and inferior temporal arteries (STA and ITA) and veins (STV and ITV) in the peripapillary area were measured. Visual field defects were categorized, and statistical analyses were performed to correlate retinal vessel calibers with field defect locations. Results Participants had a mean age of 89.68 years, with 72% male. Visual field defects included superior arcuate scotoma (20%), inferior arcuate scotoma (32%), double arcuate scotoma (30%), and tubular vision (18%). Significant vessel caliber changes were observed: for superior hemifield defects, the mean STA: ITA ratio was 1.15 (p = 0.001), and for inferior defects, it was 0.94 (p = 0.04). STV: ITV ratios also showed significant changes corresponding to visual field defects. Eyes with defects in both hemifields showed pronounced narrowing, particularly in inferotemporal vessels. Conclusions Decreased retinal vessel caliber is significantly associated with visual field defects in primary open-angle glaucoma and can be a valuable diagnostic parameter tool for assessing glaucomatous damage and the progression and severity of POAG.