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Disc haemorrhage associated with an enlarged peripapillary intrachoroidal cavitation in a non-glaucomatous myopic eye: a case report

Cited 3 time in Web of Science Cited 3 time in Scopus
Authors

Lee, Kyoung Min; Lee, Eun Ji; Lee, Seung Hyen; Kim, Tae-Woo

Issue Date
2015-10-29
Publisher
BioMed Central
Citation
BMC Ophthalmology, 15(1):145
Keywords
Disc haemorrhagePeripapillary intrachoroidal cavitationOptical coherence tomographyMyopia
Description
This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made.
Abstract
Abstract

Background
Disc haemorrhage (DH) is considered a characteristic sign of glaucoma, but its causative mechanism remains to be determined. We present a case of DH that occurred in association with an enlarged peripapillary intrachoroidal cavitation in a non-glaucomatous eye.


Case presentation
A 35-year-old woman was evaluated for a DH that had been detected during a preoperative examination for myopic refractive surgery. Enhanced depth imaging spectral-domain optical coherence tomography imaging of the optic nerve revealed a peripapillary intrachoroidal cavitation adjacent to the DH. The DH was also present at the 1-year follow-up, but had been completely absorbed at the 2-year follow-up, respectively with an enlargement and shrinkage of the intrachoroidal cavitation and prelaminar tissue schisis. Glaucomatous optic nerve change was not observed during the entire follow-up.


Conclusion
DH can be caused by mechanical damage to capillaries from microscopic changes in peripapillary tissues such as enlargement of the intrachoroidal cavitation, regardless of the presence of glaucoma.
Language
English
URI
https://hdl.handle.net/10371/100577
DOI
https://doi.org/10.1186/s12886-015-0143-7
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