Abstract
PurposeTo report structural changes observable in in vivo confocal microscopy (IVCM) in keratoconic corneas 400 μm treated with hypotonic riboflavin and collagen crosslinking (CXL).MethodsTen eyes of ten patients with progressive keratoconus and corneal thickness between 350 and 399 μm underwent CXL with hypotonic riboflavin. IVCM was performed preoperatively and at one month, three months, and six months after the procedure.ResultsIVCM analysis one month postoperatively showed complete absence of the subepithelial nerve plexus with gradual regeneration over six months in 8 of the 10 eyes, and poor regeneration in the remaining 2 eyes. The anterior stroma showed extracellular lacunae and hyper-reflective cytoplasm in a honeycomb appearance signifying edema at one month which gradually decreased over six months post CXL. Stromal keratocyte apoptosis was evident in the anterior stroma in all cases and extended to the posterior stroma in four eyes with gradual regeneration evident at three and six months. The specular endothelial count decreased by 8% (P = 0.005) post-CXL, but no corneas developed clinical signs of endothelial trauma.ConclusionIVCM analysis of thin corneas after hypotonic CXL showed posterior corneal structural changes. Posterior stromal changes were accompanied by a decrease in the endothelial cell count. This case series was a preliminary feasibility study that might necessitate conducting a well-designed controlled study.
Highlights
Keratoconus is a noninflammatory degenerative condition of the cornea, characterized by progressive corneal thinning and steepening.[1]
It is a simple technique in which riboflavin and ultraviolet A (UVA) light is applied to the eye; this treatment is postulated to increase the biochemical and biomechanical stability of the cornea[5] by stimulating the CXL.[6, 7]
Anterior keratocyte density was markedly reduced after CXL and subsequently increased but did not return to normal by the six-month postoperative visit
Summary
Keratoconus is a noninflammatory degenerative condition of the cornea, characterized by progressive corneal thinning and steepening.[1] Though the exact etiology is unknown, alterations in the corneal collagen structure[2, 3] and degree of collagen crosslinking (CXL) leads to a structurally weakened corneal tissue.[4] The spectrum of disease can range from mild astigmatism to severe ectasia requiring corneal transplantation. CXL is a popular method for management of keratoconus. Hypotonic riboflavin hydrates the stromal corneal layer, which should theoretically prevent penetration of the CXL treatment to the endothelium.[12]
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