New Findings in Early-Stage Keratoconus: Lamina Cribrosa Curvature, Retinal Nerve Fiber Layer Thickness, and Vascular Perfusion

Abstract

PurposeOur aim was to investigate the involvement of posterior pole structures in eyes affected by keratoconus (KC). Optical coherence tomography (OCT) and OCT angiography (OCTA) were used to determine the status of lamina cribrosa (LC), peripapillary retinal nerve fiber layer (RNFL), macular and peripapillary microvasculature. DesignObservational, cross-sectional, case-control analysis. MethodsSingle-center investigation involving patients with KC and healthy control subjects. Enrolled subjects underwent anterior segment OCT combined with Placido-disk topography, macular and optic nerve head swept-source OCT and swept-source OCTA scans, and 3D wide glaucoma module for peripapillary RNFL thickness measurement. The LC curvature index was used to express the degree of LC posterior bowing. We calculated the vessel density and vessel length density at the macular superficial capillary plexus, deep capillary plexus, choriocapillaris, and nerve radial peripapillary capillary plexus. ResultsOverall, 32 eyes with KC and an equal number of age- and axial length–matched control eyes were included in the analysis. Almost all (97%) of eyes with KC were classified as early stage. KC displayed a reduction in peripapillary RNFL thickness (104.8 ± 11.9 µm vs 110.7 ± 10.5 µm; P = .039) and nerve radial peripapillary capillary plexus vessel density (46.31% ± 3% vs 43.82% ± 4%; P = .006) when compared with control subjects; these differences were more evident in the temporal sector and were associated with a higher LC curvature index (9.9% ± 2.6% vs 8.48% ± 1.7%; P = .012). Mean macular superficial capillary plexus vessel density was 3 percentage points lower in eyes with KC than in healthy controls (P < .001). ConclusionEarly-stage KC may be characterized by a posterior bowing of the LC along with a subtle peripapillary RNFL thinning and vascular impairment. These findings support the hypothesis that KC may be a corneal manifestation of a more generalized “eye collagen disease.”