KERATOCONUS MANAGEMENT WITH CORNEAL COLLAGEN CROSSLINKING (Epi-on): A CASE REPORT

Abstract

Keratoconus is a progressive, non-inflammatory, degenerative disorder, most commonly bilateral, that affects the cornea. Structural alterations in corneal collagen lead to thinning and protrusion of the corneal tissue. Patients typically present with progressive corneal thinning, biomechanical weakening, and irregularities, resulting in induced myopia, irregular astigmatism, and reduced visual acuity. The prevalence of keratoconus is estimated at approximately 1 in 2000 individuals, with a male predominance. The disease usually manifests during puberty and progresses with variable dynamics into the third or fourth decade of life, ranging from mild irregular astigmatism to severe corneal protrusion. The risk of contralateral eye involvement is highest within the first years following disease onset. On the slit-lamp examination, keratoconus presents with a range of characteristic findings depending on the stage of disease progression. Early clinical signs may include subtle corneal thinning, irregular reflection on the corneal surface, and scissoring of the red reflex during retinoscopy. With disease progression, more specific signs may appear, such as: Fleischerʼs ring – iron deposition at the base of the cone, best visualized with cobalt-blue illumination, Vogtʼs striae-fine vertical stress lines in the deep stroma and Descemetʼs membrane, which disappear with gentle pressure on the globe, Increasing corneal protrusion, often best appreciated with profile examination of the cornea, localized stromal thinning, most commonly in the paracentral region, Munsonʼs sign-V-shaped indentation of the lower eyelid on downgaze, observed in advanced stages. In servere cases, acute corneal hydrops may occur due to a rupture in Descemetʼs membrane, resulting in sudden corneal edema, pain, and marked decrease in vision. The aim of this study is to present a case of bilateral keratoconus, demonstrating improvement in keratometric, visual, and ectasia parameters in the treated eye following corneal collagen crosslinking at a 3-month follow-up, and disease progression in the untreated fellow eye.