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Published on: September 12, 2014
Use of autologous serum in corneal epithelial defects post-lamellar surgery
Salomon Esquenazi1, Jiucheng He, Haydee E P Bazan
1Department of Ophthalmology and Neuroscience Center of Excellence, LSU Health Sciences Center, New Orleans, LA 70112, USA. sesque@lsuhsc.edu
Purpose:
To evaluate the efficacy of an autologous serum treatment of post-LASIK (laser in situ keratomileusis) corneal epithelial defects in a rabbit model.
Methods:
Five milliliters blood samples from 10 New Zealand rabbits were obtained by venepuncture. The serum was aseptically separated and diluted with saline solution to 20%. The final preparation was placed into 3-mL bottles with ultraviolet protection and maintained at 4 degrees C. Corneas were de-epithelialized using a 7-mm optical zone marker. A 160-microm thick flap was created in both eyes of all rabbits using an automatic corneal shaper microkeratome. Right eyes were treated with serum drops 6 times per day. Left eyes were treated with preservative-free artificial tears. Vital staining of the ocular surface and the area of corneal epithelial defect was measured daily for 1 week. Rabbits were humanely euthanized at postoperative day 7, and corneas were fixed and sectioned. Hematoxylin and eosin staining and immunohistochemical analysis were performed.
Results:
Corneas treated with autologous serum had a statistically significant increase in the epithelial healing rate compared with those treated with artificial tears. Serum-treated corneas showed significantly less terminal transferase-mediated dUTP nick-end labeling (TUNEL) staining in the interface, minimal inflammatory cell infiltration, and less induced synthesis of stromal chondroitin sulfate than did corneas treated with preservative-free artificial tears.
Conclusions:
Treatment with autologous serum could be an efficient way to provide essential components to the ocular surface in the treatment of post-LASIK epithelial defects. Autologous serum induces faster epithelial healing than do artificial tears, leading to (1) a decrease in keratocyte apoptosis and migration of fibroblasts and myofibroblasts in the wound site, (2) a decrease in the migration of inflammatory cells, and (3) a consequent inhibition of cytokine release. This treatment could improve long-term refractive results post-LASIK.
