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Contact lens induced corneal vascularisation — Aetiology and risk factors
Contact Lens Induced Corneal Vascularisation - - Aetiology and Risk Factors Charles W. McMonnies
Charies McMonnies ts an Optometrist in prtvate practice in Sydney and is in volved in teaching and research at C. C.L.R. U., University of New South Wales. (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
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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 l m m from the limit of visible iris in normal corneas, especially at t h e 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. A t 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
Journal of the British Contact Lens Association Vol. 7. No. 3
questions are not known and speculation regarding aetiology and risk factors must be based on studies of corneal vascularisation outside the contact lens field, as there have been few studies involving contact lenses as an experimental stimulus to corneal vasculadsation. Ethical considerations limit the scope of experiments on human subjects but some rabbit studies have been published for example Dixon and Lawaczeck (1963) and Duffin, Weissman, Glasser and Pettit (1982)). However these experiments involved the continuous wear of hard contact lenses on unadapted eyes, and apart from differences between rabbit and human corneas, such strong stimuli to corneal vascularisation may not be relevant to the incidence of this complication of contact lens wear in adapted human subjects. In the absence of other information, speculation regarding risk fitting factors must serve as the only guide to contact lens practitioners in their attempts to manage this complication. Ruben (1981) Larke Humphreys and Holmes (1981) and McMonnies (1984), for example, have attempted to describe contact lens mechanisms of new vessel growth and so show the contact lens fitting factors that give the greatest risk. McMonnies (1984) proposed that contact lenses are more likely t O cause corneal vascularisation in patients who are more susceptible tO this complication, especially if the lenses are oversown, and if the lenses are associated with peripheral Corneal oedema, epithelial disturbance~ episodes of acute inflammation, chronic hypoxic metabolosm, restricted venous drainage or any other cause of chronic limbal hyperaemia. McMonnies (1984) concluded that thick hydrogel lenses may be more likely to cause corneal vascularisation than do hard contact lenses, if they cause greater amounts of peripheral corneal oedema a n d / o r if they restrict venous drainage to a greater extend a n d / o r if they result in more chronic limbal hyperaemia or more frequent episodes of acute limbal hyperaemia. Therapeutic fittings aside, incidence of contact lens induced corneal vascularisation in patients fitted for the correction of refractive errors is not very high, but occasionally serious cases occur. Obviously stromal vascularisation is more serious than superficial vessel growth as it indicates a deeper location of the insult. As well vascularisation in young contact lens wearers is a more grave complication with the risk of a greater opportunity for further change over a longer prospective period of contact lens wear. It is probable that contact lens induced corneal vascularisation occurs because of varying combinations of adverse fitting factors in patients with increased susceptibility for this complication because of varying combinations of systemic and personal factors. For example, systemic conditions such as lupus erythematosis or nutritional deficiency, may predispose a contact lens wearer to this complication. Perhaps ocular factors such as tear deficiency, chronic allergy or
156
acne rosacea have a predisposing effect. Perhaps personal factors relating to chronic ocular irritation from the excess use of cosmetics or long term exposure to adverse environmental conditions have a predisposing role. Perhaps vision factors are significant if patients have a dependancy on their contact lenses and overwear them because spectacles are an inferior form of correction (keratoconus and aphakia for example). Perhaps the patient with a psychological dependency on contact lenses, because of their intense dislike and rejection of spectacles, is more likely to have this complication because contact lenses are overworn. There is a great deal not known about contact lens induced corneal vascularisation. It is not known how often it occurs. It is not known which fitting factors such as lens type or maintenance method are mostly likely to lead to its development. It is not known which patients are more susceptible or which wearing conditions are the most likely to cause this complication. It is known that corneal vascularisation is a serious contact lens complication leading to permanent change in the capacity of the cornea to be involved in immune diseases including increased risk of graft rejection should such surgery become necessary. Overwear of soft lenses of limited gas permeability is a combination of conditions that is seen to occur clinically in ass~iation with corneal stromal vascularisation, McMonnies (1983), Niramkari e t a1(1983). Perhaps it is because ~da~ lenses~cause greater amounts of peripheral oedem~; a n d / o r reduction in the" elimination of waste p r o s because of restricted venous outflow, a n d / o r chronic levels of limbal injection. Perhaps under such circumstances, overwear allows insufficient time for corneal recovery from these and other forms of contact lens insult, so that corneal vascularisation ensues. It may be that contact lens fitting in general has improved sufficiently already, or will improve sufficiently in the future, for contact lens induced corneal vascularisation to become such a rare finding that its aetiology and an appreciation of the risk fitting factors remain speculative. However it behoves each practitioner to be aware of possible casual factors with current lenses so that appropriate preventative steps can be employed.
References Dixon, J.M. and Lawaczeck, E. (1963), Corneal vascularisation due to contact lenses, Archives of Ophthalmology, 69, 72-75. Duffin, M.R., Weissman, B.A., Glasses, D.B. and Pettit, T.H. (1982), Flurbiprofen in the treatment of corneal neovascularisation induced by contact lenses, American Journal of Ophthalmology , 93607-614.
Journal of the British Contact Lens Association Vol. 7 No. 3
Duke-Elder, S. and Leigh, A.G. (1977), System of ophthalmology, Volume VIII, Diseas of the outer eye, Part 2, London, Henry Kimpton, 676-691. Larke, J.R., Humphreys, J.A. and Holmes, R. (1981), Apparent corneal neovascularisation in soft lens wearers, Journal of the British Contact Lens Association, 4, 105-106. McMonnies, C.W., Chapman-Davies, A. and Holden, B.A. (!982), The vascular response to contact lens wear, American Journal of Optometry, 59 (10), 795-799. McMonnies, C.W. (1983), Contact lens induced corneal vascularisation, International Contaft Lens Clinic, 10 (1), 12-21. McMonnies, C.W. (1984), Risk factors in the aetiology of contact lens induced corneal vascularisation, International Contact Lens Clinic, 11 (1).
Journal of the British Contact Lens Association Vol. 7. No. 3
Nirankari, V.S., Karesh, J., Lakhanpal, V. and Richards, R.D. (1983), Deep stromal vascularisation associated with cosmetic, daily-wear contact lenses, Archives of Ophthalmology 101, 46-47. Ruben, M. (1981), Corneal vascularisation in complications of contact lenses, International Ophthalmology Clinics, 21 (2) 27-38.
Address for further correspondence: 3rd Floor, State Building, 49 Market Street, Sydney, N.S.W.
157
Charies McMonnies ts an Optometrist in prtvate practice in Sydney and is in volved in teaching and research at C. C.L.R. U., University of New South Wales. (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
154
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 l m m from the limit of visible iris in normal corneas, especially at t h e 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. A t 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
Journal of the British Contact Lens Association Vol. 7. No. 3
questions are not known and speculation regarding aetiology and risk factors must be based on studies of corneal vascularisation outside the contact lens field, as there have been few studies involving contact lenses as an experimental stimulus to corneal vasculadsation. Ethical considerations limit the scope of experiments on human subjects but some rabbit studies have been published for example Dixon and Lawaczeck (1963) and Duffin, Weissman, Glasser and Pettit (1982)). However these experiments involved the continuous wear of hard contact lenses on unadapted eyes, and apart from differences between rabbit and human corneas, such strong stimuli to corneal vascularisation may not be relevant to the incidence of this complication of contact lens wear in adapted human subjects. In the absence of other information, speculation regarding risk fitting factors must serve as the only guide to contact lens practitioners in their attempts to manage this complication. Ruben (1981) Larke Humphreys and Holmes (1981) and McMonnies (1984), for example, have attempted to describe contact lens mechanisms of new vessel growth and so show the contact lens fitting factors that give the greatest risk. McMonnies (1984) proposed that contact lenses are more likely t O cause corneal vascularisation in patients who are more susceptible tO this complication, especially if the lenses are oversown, and if the lenses are associated with peripheral Corneal oedema, epithelial disturbance~ episodes of acute inflammation, chronic hypoxic metabolosm, restricted venous drainage or any other cause of chronic limbal hyperaemia. McMonnies (1984) concluded that thick hydrogel lenses may be more likely to cause corneal vascularisation than do hard contact lenses, if they cause greater amounts of peripheral corneal oedema a n d / o r if they restrict venous drainage to a greater extend a n d / o r if they result in more chronic limbal hyperaemia or more frequent episodes of acute limbal hyperaemia. Therapeutic fittings aside, incidence of contact lens induced corneal vascularisation in patients fitted for the correction of refractive errors is not very high, but occasionally serious cases occur. Obviously stromal vascularisation is more serious than superficial vessel growth as it indicates a deeper location of the insult. As well vascularisation in young contact lens wearers is a more grave complication with the risk of a greater opportunity for further change over a longer prospective period of contact lens wear. It is probable that contact lens induced corneal vascularisation occurs because of varying combinations of adverse fitting factors in patients with increased susceptibility for this complication because of varying combinations of systemic and personal factors. For example, systemic conditions such as lupus erythematosis or nutritional deficiency, may predispose a contact lens wearer to this complication. Perhaps ocular factors such as tear deficiency, chronic allergy or
156
acne rosacea have a predisposing effect. Perhaps personal factors relating to chronic ocular irritation from the excess use of cosmetics or long term exposure to adverse environmental conditions have a predisposing role. Perhaps vision factors are significant if patients have a dependancy on their contact lenses and overwear them because spectacles are an inferior form of correction (keratoconus and aphakia for example). Perhaps the patient with a psychological dependency on contact lenses, because of their intense dislike and rejection of spectacles, is more likely to have this complication because contact lenses are overworn. There is a great deal not known about contact lens induced corneal vascularisation. It is not known how often it occurs. It is not known which fitting factors such as lens type or maintenance method are mostly likely to lead to its development. It is not known which patients are more susceptible or which wearing conditions are the most likely to cause this complication. It is known that corneal vascularisation is a serious contact lens complication leading to permanent change in the capacity of the cornea to be involved in immune diseases including increased risk of graft rejection should such surgery become necessary. Overwear of soft lenses of limited gas permeability is a combination of conditions that is seen to occur clinically in ass~iation with corneal stromal vascularisation, McMonnies (1983), Niramkari e t a1(1983). Perhaps it is because ~da~ lenses~cause greater amounts of peripheral oedem~; a n d / o r reduction in the" elimination of waste p r o s because of restricted venous outflow, a n d / o r chronic levels of limbal injection. Perhaps under such circumstances, overwear allows insufficient time for corneal recovery from these and other forms of contact lens insult, so that corneal vascularisation ensues. It may be that contact lens fitting in general has improved sufficiently already, or will improve sufficiently in the future, for contact lens induced corneal vascularisation to become such a rare finding that its aetiology and an appreciation of the risk fitting factors remain speculative. However it behoves each practitioner to be aware of possible casual factors with current lenses so that appropriate preventative steps can be employed.
References Dixon, J.M. and Lawaczeck, E. (1963), Corneal vascularisation due to contact lenses, Archives of Ophthalmology, 69, 72-75. Duffin, M.R., Weissman, B.A., Glasses, D.B. and Pettit, T.H. (1982), Flurbiprofen in the treatment of corneal neovascularisation induced by contact lenses, American Journal of Ophthalmology , 93607-614.
Journal of the British Contact Lens Association Vol. 7 No. 3
Duke-Elder, S. and Leigh, A.G. (1977), System of ophthalmology, Volume VIII, Diseas of the outer eye, Part 2, London, Henry Kimpton, 676-691. Larke, J.R., Humphreys, J.A. and Holmes, R. (1981), Apparent corneal neovascularisation in soft lens wearers, Journal of the British Contact Lens Association, 4, 105-106. McMonnies, C.W., Chapman-Davies, A. and Holden, B.A. (!982), The vascular response to contact lens wear, American Journal of Optometry, 59 (10), 795-799. McMonnies, C.W. (1983), Contact lens induced corneal vascularisation, International Contaft Lens Clinic, 10 (1), 12-21. McMonnies, C.W. (1984), Risk factors in the aetiology of contact lens induced corneal vascularisation, International Contact Lens Clinic, 11 (1).
Journal of the British Contact Lens Association Vol. 7. No. 3
Nirankari, V.S., Karesh, J., Lakhanpal, V. and Richards, R.D. (1983), Deep stromal vascularisation associated with cosmetic, daily-wear contact lenses, Archives of Ophthalmology 101, 46-47. Ruben, M. (1981), Corneal vascularisation in complications of contact lenses, International Ophthalmology Clinics, 21 (2) 27-38.
Address for further correspondence: 3rd Floor, State Building, 49 Market Street, Sydney, N.S.W.
157