Contact lens induced corneal vascularisation — Aetiology and risk factors

Abstract

(This paper was read at Brighton by Christopher Kerr. ) Duke Elder and Leigh (1965) described three stages of new corneal vessel growth. Firstly, the filling of terminal capillaries that are normally empty, followed by a stage of active vessel growth, and finally a stage of established comeal vessels. The first stage occurs in contact lens wear when inflammatory responses to physical, physiological and chemical trauma occur. Those inflammatory responses provide a useful index of the degree of acceptance of the contact lens, its method of use and management. However a practitioner may have difficulty in the assessment of limbal injection because of the lack of reliable methods of clinically quantifying inflammatory response. Larke Humphreys and Holmes (1981) have confirmed that chronic limbal hyperaemia is common amongst contact lens wearers. McMonnies, ChapmanDavies and Holden (1982) measured red free photographs to determine the degree of filling of limbal vessels in groups of old and young non contact lens wearers, and compared these with separate groups of hard and soft lens wearers. Their results also showed that contact lens wearers sustain significantly higher levels of limbal injection, especially soft lens wearers. Of course the results may be different if the groups compared wore contact lenses that were more gas permeable, or which were less bound with sensitising preservatives. It is sound practice to recognise the possibility that chronic injection may be a precursor of corneal vascularisation in susceptible individuals, especially perhaps if there are episodes of acute inflammation. Remedial steps should be taken to reduce chronic limbal injection so that the risk of advancing to a stage of active vessel growth is minimised. Corneal vascularisation has been reported in association with all types of contact lens but there is no reliable estimate of its incidence. A principle difficulty is the clinical definition of vascularisation as distinct from the filling of limbal capillaries that are normally empty. McMonnies (1983) reviewed these problems and described how terminal limbal capillaries may appear to be corneal vessels when they are in transitional conjunctival tissue that overlays the transparent corneal stroma. The degree of overlay (and so apparent corneal vascularisation) can extend over transparent stroma by as much as lmm from the limit of visible iris in normal corneas, especially at the superior limbus where the degree of overlay can be aS great as 2.0mm from the limit of visible iris. Ideally, limbal vessels in contact lens wearing eyes should be empty, but even when injection is noted during after-care, the above limits of apparent vessel incursion into the cornea should not be exceeded and alteration to the contact lens fitting is indicated because chronic limbal injection may be a precursor to new vessel growth. Greater concern is registered when signs of new vessel growth are observed. For example budding/sprouting/spike formations may be seen to extend from existing vessels surrounded by exudate and cellular infiltrates. In such cases immediate remedial action should be taken to relieve the stimulus to new vessel growth. At any stage of contact lens induced corneal vascularisation, the ability of clinicians to take appropriate remedial action (apart from abstinence from lens wear)is limited by lack of knowledge of the precise stimuli and conditions for new vessel growth. What are the aetiological fitting factors and which are the at risk patients? Unfortunately the answers to these