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Journal of Ophthalmology
Volume 2017 (2017), Article ID 5614089, 11 pages
Research Article

A Surgical Cryoprobe for Targeted Transcorneal Freezing and Endothelial Cell Removal

1Structural Biophysics Research Group, School of Optometry and Vision Sciences, Cardiff University, Maindy Road, Cardiff CF24 4HQ, UK
2Department of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, 1-3 Miyakodami-Tatara, Kyoto 610-0321, Japan
3Division of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University, Lancaster LA1 4YQ, UK
4Network Medical Products Ltd. Coronet House, Kearsley Road, Ripon, North Yorkshire HG4 2SG, UK
5Department of Frontier Medical Science and Technology for Ophthalmology, Kyoto Prefectural University of Medicine, Hirokoji-Kawaramachi, Kyoto 602-0841, Japan

Correspondence should be addressed to Andrew J. Quantock

Received 13 December 2016; Accepted 13 February 2017; Published 16 May 2017

Academic Editor: Neil Lagali

Copyright © 2017 Alina Akhbanbetova et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Purpose. To examine the effects of transcorneal freezing using a new cryoprobe designed for corneal endothelial surgery. Methods. A freezing console employing nitrous oxide as a cryogen was used to cool a series of different cryoprobe tip designs made of silver for high thermal conductivity. In vitro studies were conducted on 426 porcine corneas, followed by preliminary in vivo investigations on three rabbit corneas. Results. The corneal epithelium was destroyed by transcorneal freezing, as expected; however, the epithelial basement membrane remained intact. Reproducible endothelial damage was optimally achieved using a 3.4 mm diameter cryoprobe with a concave tip profile. Stromal edema was seen in the pre-Descemet’s area 24 hrs postfreeze injury, but this had been resolved by 10 days postfreeze. A normal collagen fibril structure was seen 1 month postfreeze, concurrent with endothelial cell repopulation. Conclusions. Transcorneal freezing induces transient posterior stromal edema and some residual deep stromal haze but leaves the epithelial basement membrane intact, which is likely to be important for corneal re-epithelialization. Localized destruction of the endothelial monolayer was achieved in a consistent manner with a 3.4 mm diameter/concave profile cryoprobe and represents a potentially useful approach to remove dysfunctional corneal endothelial cells from corneas with endothelial dysfunction.