Atropine penalization for "rescuing" patching failures.

OS. Examination revealed enlargement of the epithelial defect, with 50% stromal thinning nasally and inferonasally, without an apparent infiltrate (Figure 2). Corneal culture was positive for Corynebacterium pseudodiptheriticum in the enrichment broth only. A course of fortified antibiotic agents did not improve the clinical findings; there was further thinning of the stroma and impending perforation. The patient was then referred to The Wilmer Eye Institute Ocular Surface Diseases and Dry Eye Clinic. A review of systems was positive for dry mouth and significant joint problems. Serologic testing showed positive antinuclear, anti-Ro, and antiphospholipid antibodies; a low C3 level; and an elevated erythrocyte sedimentation rate. The patient was subsequently diagnosed as having primary SS. He was admitted to the hospital for pulse intravenous corticosteroid treatment, with transition to oral corticosteroids and hydroxychloroquine sulfate, as well as topical cyclosporine, 1%, and medroxyprogesterone acetate, 1%. One week later, amniotic membrane grafting was performed, and it was repeated 2 weeks later along with a tarsorrhaphy. After 6 weeks of cyclosporine treatment, his visual acuity was counting fingers at 30 cm with a failed graft, but there was no epithelial defect. Comment. Sterile corneal melt in patients with primary or secondary SS is well recognized and has been reported after cataract surgery and conductive keratoplasty. To our knowledge, these are the first reported cases of corneal melt after DSEK. Both patients had previously undiagnosed SS. This syndrome is known to be widely underdiagnosed, especially in the male population and when ocular findings are the initial symptoms. The corneal lesions associated with SS are characteristically painless epithelial defects and stromal ulcerations without an apparent infiltrate; they are commonly located in the central or paracentral regions of the cornea. The exact pathogenesis is not fully established and may involve the underlying inflammatory process, aqueous tear deficiency, denervation of the cornea from surgical trauma, or the use of topically administered medications that cause epithelial toxic effects or delayed healing. Mechanical epithelial scraping alone can also cause immediate damage to underlying anterior keratocytes, leading to their degeneration, and may have contributed to the development of corneal melting in both patients. Although DSEK is known for maintaining corneal surface integrity, sterile corneal melt can occur, especially in patients with chronic dry eye syndrome. Therefore, it is prudent to perform a detailed review of systems and laboratory investigations as needed to uncover possible underlying collagen vascular disorders before any corneal surgery. Scraping of the epithelium should be avoided in patients with significant aqueous tear deficiency. Because systemic and local interventions are necessary in the treatment of these patients, a rheumatology consultation should be obtained promptly for appropriate management.