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Updated: Jun 21, 2026
Corneal Donor Tissue Preparation for Descemet's Membrane Endothelial Keratoplasty
Published on: September 17, 2014
Failed descemet-stripping automated endothelial keratoplasty grafts: a clinicopathologic analysis
Julia Shulman1, Mark Kropinak, David C Ritterband
1Department of Ophthalmology, The New York Eye and Ear Infirmary, New York, NY 10003, USA.
Purpose:
To describe the clinicopathologic findings in failed Descemet-stripping automated endothelial keratoplasty (DSAEK) grafts.
Design:
Retrospective, interventional case series.
Setting:
New York Eye and Ear Infirmary.
Study Population:
Twenty-one patients with 22 failed DSAEK grafts treated between March 1, 2006 and February 1, 2008.
Intervention:
Repeat DSAEK or penetrating keratoplasty were performed in the eyes with failed grafts. All failed grafts were examined histopathologically.
Main Outcome Measures:
Histopathologic parameters studied in failed DSAEK grafts included endothelial cell count, interface characteristics, retrocorneal membrane formation, inflammation, and immunoreactivity for herpes simplex virus type 1 (HSV-1) antigen.
Results:
DSAEK failure was strongly associated with postoperative lenticle dislocation. Graft failure was primary in 19 DSAEKs and secondary to rejection, eccentric trephination with epithelial ingrowth, or bacterial infection in the remaining 3. All failed grafts demonstrated endothelial hypocellularity and stromal edema. Additional findings included stromal inflammation (68%), interface fibrosis (50%), retrocorneal membrane (36%), unplanned retention of Descemet membrane (14%), immunoreactivity for HSV-1 (14%), paucicellular stroma (14%), and uneven trephination with epithelial ingrowth (5%).
Conclusions:
Most DSAEK failures are secondary to endothelial cell loss. Other contributing factors include interface fibrosis, retrocorneal membrane formation, retained host Descemet membrane, uneven trephination, epithelial ingrowth, graft rejection, and infection.
