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Alina Akhbanbetova, Shinichiro Nakano, Stacy L Littlechild, Robert D Young, Madara Zvirgzdina, Nigel J Fullwood, Shigeru Kinoshita, Naoki Okumura, Noriko Koizumi, Andrew J Quantock; A Surgical Cryoprobe for Targeted Transcorneal Freezing to Treat Corneal Endothelial Dysfunction. Invest. Ophthalmol. Vis. Sci. 2016;57(12):1248.
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© ARVO (1962-2015); The Authors (2016-present)
To examine the effects on corneal tissue of localized freezing induced by a new surgical cryoprobe. The machine was designed to remove endothelial cells from the posterior surface of the cornea in a reproducible and targeted manner to aid the treatment of corneal endothelial dysfunction.
A freezing console was designed and manufactured based on the use of nitrous oxide as a cryogen. The console was connected to one of four different cryoprobes, each with a different freezing tip (1.8 mm-diameter, flat profile; 2.4 mm-diameter, flat profile; 2.4 mm-diameter concave profile; 3.4 mm-diameter, concave profile) at which temperatures below -50°C were achieved. In vitro studies were conducted on 426 porcine corneas, followed by a small number of in vivo investigations on rabbit corneas. After treatment the epithelial basement membrane, corneal stroma, and corneal endothelium were investigated by slit-lamp microscopy, ultrasound pachymetry, and light and electron microscopy.
In vivo and in vitro the corneal epithelium was destroyed by freezing, but the epithelial basement membrane remained intact. In vitro, reproducible corneal endothelial damage was achieved using the 3.4 mm-diameter cryoprobe tip with the concave profile. The damage occurred after a short, 3-sec freeze, and was confined to a circular region of the endothelium located directly under the surface application position of the cryoprobe tip. Corneal edema was seen in vivo 24-hrs after freeze injury and was accompanied by alterations to the arrangement of collagen fibrils, but this resolved by 10-days and 1-month concurrent with endothelial repopulation of the wound area.
Surface corneal freezing using a 3.4 mm-diameter concave cryoprobe induces transient stromal edema, but leaves the epithelial basement membrane intact which likely aids epithelial resurfacing. Localized destruction of the endothelial monolayer was achieved in a consistent manner, and represents a potentially useful approach to help treat corneal endothelial dysfunction.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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