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Corneal vascularisation and contact lenses.

EDITORIAL The cornea is avascular for the simple reason that to be otherwise would compromise its role as the primary refracting surface of the eye. As a result, situations that may cause vascularisation of this beautifully transparent tissue are energetically avoided. Visual disturbance caused by vascular encroachment upon the central cornea region is, perhaps, the most obvious threat. However, corneal vascula-risation (CV) has other potentially damaging consequences including jeopardizing the normally immune privileged status of the anterior chamber (1) and increasing the risk of graft rejection (2,3). For the general population, the most likely situation in which CV will be encountered is in association with contact lenses. Although prevalence estimates are quite variable, the suggestion is that between a tenth and a third of all cases of CV have contact lens involvement. Not all lenses are equal in this respect however. Prevalence figures tend to hide the fact that rigid gas permeable (RGP) lenses are much less likely to be associated with CV than are soft contact lenses (SCL). Although the mechanisms whereby contact lenses cause CV are not completely understood, the divergent responses to the various lens types are instructive and consideration of the functional differences between these modalities can provide valuable aetiological insight. Typical RGP diameters are in the region of 9-10mm and consequently cover only the central portion of the cornea during wear. Conversely, SCLs are substantially larger, at around 13-15 mm, and cover the entire cornea as well as the limbus and some of the surrounding peri-limbal conjunctiva. The general effect of this additional coverage with SCLs is to reduce access of the underlying tissues to oxygen from the atmosphere and that dissolved in the tear film. As a result, the peripheral cornea and limbus are likely to experience some degree of hypoxia. An early manifestation of this is hyperae-mia within the limbal vessels, a response that has been recognized for many years during SCL wear and one that is directly associated with the hypoxia they produce (4). Although there is debate about whether peripheral hypoxia is a sufficient stimulus in itself to cause CV, the associated short term vas-cular changes are apparently identical to those seen where CV does eventually occur. One other key aspect of lens wear that impacts CV is the mode of use. Wearing lenses for long periods of time, and particularly during periods of sleep, i.e. extended or continuous wear, carries …