Donor corneal stroma and host–donor interface vascularization after Descemet’s membrane stripping with automated endothelial keratoplasty

Editor, S ince its introduction in 1999 (Melles et al. 1999), endothelial keratoplasty has evolved rapidly as an alternative to penetrating keratoplasty. A popular modification of the original technique is now referred to as Descemet’s membrane stripping with automated endothelial keratoplasty (DSAEK) (Gorovoy 2006). Given the relative novelty of the procedure, little data are available regarding postoperative complications. To our knowledge, donor corneal stroma and host–donor interface vascularization after endothelial keratoplasty have not been reported in the literature. The patient was an 86-year-old woman with a history of enucleation of the left eye. In her right eye, she had undergone cataract surgery 25 years previously and tube shunt surgery for advanced normal tension glaucoma both 10 years and 2 years previously. She also had a history of uveitis of unknown aetiology 3 years previously; this was controlled by topical corticosteroid therapy with no subsequent recurrence. Full systemic work-up was negative. Six months after the second tube shunt surgery, she had a visual acuity of 3 ⁄200 and central corneal thickness of 804 lm. Examination revealed severe corneal oedema emanating superatemporally where the tube shunt was in touch with the corneal endothelium. There was no evidence of corneal scarring or vascularization. The anterior chamber was quiet with no evidence of cell or flare. She underwent DSAEK. At the same time the tube shunt was trimmed farther back into the angle. The donor cornea had 2994 endothelial cells ⁄mm. The eye bank donor information sheet indicated no stromal abnormality. Five months after DSAEK the patient developed a corneal ulcer that responded to topical antibiotic therapy. Bacterial and fungal cultures taken initially were negative. After resolution of the ulcer, she developed a dense central corneal opacity and 40% thinning. Deep corneal vascularization developed during the acute phase of the corneal ulcer (i.e. during the infiltrate and its resolution). Her visual acuity dropped to counting fingers at a distance of 1 foot. She underwent penetrating keratoplasty 10 months after DSAEK. Histopathological examination disclosed a corneal button with intact epithelium. Bowman membrane was absent where diffuse anterior stromal scarring was present (Fig. 1A,B). No vascularization was identified in the superficial stroma. Diffuse stromal vascularization was present in the donor stroma (Fig. 1A,B). The vascularization extended to the donor– recipient interface (Fig. 1A,B). The 90-lm-thick posterior corneal lamella was completely attached and thickened to 160 lm at the area of vascularization. Recipient Descemet’s membrane was entrapped at the interface at the other margin (Fig. 1C). The endothelium was intact with 10 nuclei per 40 · high-power field (HPF). The mechanisms of corneal vascularization are yet to be fully elucidated. Corneal angiogenic privilege is an active process involving the production of antiangiogenic factors to counterbalance the proangiogenic factors, which are upregulated after wound healing. Disruption of this delicate balance during corneal wound healing can lead to pathological corneal vascularization (Huang et al. 2005; Azar 2006). Cursiefen et al. (2006) hypothesized that vascular endothelial growth factor-receptor 3 (VEGF-R3) expression by the corneal epithelium promotes avascularity of the normal cornea by serving as a ‘sink’ for VEGF-R3 ligands. Angiogenic factors, such as basic fibroblast growth factor, endostatin and angiostatin, can be produced from the degradation of the corneal extracellular matrix during the process of wound healing. Matrix metalloproteinases and other proteolytic enzymes modulate corneal vascularization via matrix degradation to allow endothelial migration (Huang et al. 2005). We postulate that the disruption of the integrity of the corneal epithelium and the anterior stroma during the