OPTOMETRY. Corneal conjunctivalisation in long-standing contact lens wearers

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1 C L I N I C A L A N D E X P E R I M E N T A L OPTOMETRY Corneal conjunctivalisation in long-standing contact lens wearers Clin Exp Optom 2007; 90: 1: Raul Martin OD IOBA Eye Institute, School of Optometry, Department of Theoretical Physics, Atomic, Molecular and Nuclear Physics and Optics, University of Valladolid, Valladolid, Spain raul@ioba.med.uva.es Submitted: 23 March 2006 Revised: 1 June 2006 Accepted for publication: 14 June 2006 DOI: /j x Background: There are many contact lens-related ocular surface disorders. Some can damage the limbal region where stem cells are thought to be located in its basal cell layer. This damage can result in destruction and a deficiency of corneal stem cells. One important sign of this complication is corneal conjunctivalisation. The purpose of this study is to describe clinical characteristics of a series of long-standing contact lens (CL) wearers with corneal conjunctivalisation (CC). Methods: In a one-year (March 2004 to March 2005) retrospective unmasked study, 591 CL clinical histories (195 new patients and 396 review patients) were analysed. Results: There were 24 eyes of 14 myopic patients (93 per cent women) with CC without a specific disease entity known to cause limbal stem cell deficiency (LSCD). Conjunctivalisation occurred in the inferior limbus of three eyes (12 per cent). Only four patients (28.6 per cent) reported previous ocular symptoms. All were myopic with a mean spherical equivalent of ± 5.00 (SD) dioptres (range from to D) and mean visual acuity 0.9 ± 0.2 (range from 0.4 to 1.2). The mean years of CL wear was 17.6 ± 8.5 (CI 95% 13.2 to 22; range six to 30). All were daily-wear patients with a mean daily-wear time of 12.5 ± 1.8 hours per day (CI 95% 11.6 to 13.4). Conclusion: Corneal conjunctivalisation is a contact lens-related complication in asymptomatic patients. Optometrists can play an important role in early diagnosis, education and management of these patients. Key words: conjunctivalisation, corneal disease, contact lenses There are many contact lens-related ocular surface disorders. Three principal mechanisms can damage the ocular surface: mechanical rubbing especially from poorly fitting contact lenses, long-term hypoxia and toxic lens solutions. This damage can injure the limbal region where stem cells are thought to be located in its basal cell layer and it may result in destruction and a deficiency of corneal stem cells. 1,2 Classical conjunctival transdifferentiation theory is incorrect 2 and has been replaced by the limbal stem cell theory. Corneal stem cells have an infinite proliferative potential. Cell division gives rise to progeny called transient amplifying cells that have a high but limited proliferative potential. Finally, transient amplifying cells are divided more frequently into specific differentiated cells. Corneal and conjunctival epithelia are different. They have specific keratins, for example, K3 keratin is absent in conjunctival epithelium and K19 is present only in conjunctival epithelium. Limbal stem cell deficiency (LSCD) is a pathological state secondary to limbal damage. The principal characteristics are corneas with poor epithelialisation (persistent defects or recurrent erosions), chronic stromal inflammation (keratitis with scarring), corneal vascularisation and corneal conjunctivalisation (the corneal surface is covered by ingrowing conjunctival epithelium). 1 3 Patients with LSCD can 26

2 present with a range of symptoms, including irritation, photophobia and decreased visual acuity. 3,4 The diagnosis relies on laboratory tests such as impression cytology to detect the presence of goblet cells or the expression of certain types of keratin in corneal epithelium. 3,4 Corneal diseases that manifest LSCD can be subdivided into two major categories. 5 In the first, limbal epithelial stem cells are destroyed by known or recognisable agents, such as a chemical or thermal burn, Stevens-Johnson syndrome, toxic epidermal necrolysis, multiple ocular surgeries or long-term topical medications (iatrogenic), 6 severe microbial infection, radiation, anti-metabolites including 5- fluorouracil and mitomycin C, and contact lens wear. 5 The second category is characterised by a gradual loss of the stem cell population, without known or identifiable precipitating factors. In this situation, the limbal stromal niche is affected and progressively deteriorates by a variety of aetiologies that include aniridia, coloboma, neoplasia, multiple hormonal deficiencies, peripheral ulcerative corneal disease, neurotrophic keratopathy and idiopathic limbal deficiency. 1,2,5 These diseases can be categorised according to whether inheritance is a factor. The underlying pathophysiology explains why transplantation of epithelial stem cells and restoration of the limbal stem cell stromal environment (for example, by amniotic membrane transplantation or limbal transplantation) are necessary for ocular surface reconstruction in cases of severe LSCD. 2 Contact lens-induced LSCD may represent 15 per cent of LSCD 4 but there are only clinical reports describing LSCD secondary to contact lens wear. 1 We present clinical characteristics of a series of long-standing contact lens patients with corneal conjunctivalisation without a specific disease known to cause LSCD. METHODS A one-year (March 2004 to March 2005) retrospective unmasked analysis of 591 consecutives contact lens patient records (195 new and 396 review patients) was conducted to determine those with corneal conjunctivalisation secondary to contact lens use and their clinical characteristics. One optometrist reviewed all patients. The clinical protocol (IOBA Optometry Unit) includes a detailed history of contact lens-related symptoms (red eye, dryness, itching, pain, irritation, photophobia and visual changes), visual acuity, slitlamp biomicroscopy (standard four cross scale (zero, 1+ trace, 2+ mild, 3+ moderate and 4+ severe) for findings, such us blepharitis, corneal scarring, vascularisation and fluorescein staining. Specific procedures are indicated including digital photography, late fluorescein staining (10 minutes minimum) and documentation of the presence or absence of palisades of Vogt in the limbal area with conjunctivalisation. All clinical records were evaluated. New patients were those who visited the IOBA Optometry Unit for the first time and review patients were those who wore contact lenses previously fitted in the IOBA Optometry Unit. We excluded all known aetiologies of LSCD except contact lenses wear. We compiled patient data on age, gender, duration of contact lenses wear, hours of wear per day, symptoms, visual acuity, corneal findings, ocular abnormalities and systemic disorders. Slitlamp examination was directed to the presence or absence of palisades of Vogt, corneal opacification and distribution and presence of vascularisation (more than one cross). Fluorescein staining was performed in every patient. Late fluorescein staining of the corneal surface was defined as positive (more than one cross) when noted 10 minutes later but not immediately (clinical protocol of IOBA Optometry Unit). This sign usually corresponds to the vascularised region. A descriptive statistical analysis was made to determinate means, standard deviations and confidence intervals. Calculations were performed with SPSS for Windows RESULTS Twenty-four eyes of 14 myopic patients (nine new patients and five review patients) out of the 591 had corneal conjunctivalisation (2.4 per cent, CI 95%, 1.1 to 3.5) not previously diagnosed with a specific disease known to be a cause of LSCD. Ninety-three per cent of patients were female (CI 95%, ) and only one was male. The mean age was 36.9 ± 9.1 years (CI 95%, 32 to 42, range 21 to 49). All were myopic with mean spherical equivalent of ± 5.00 D (range to D) with mean visual acuity 0.9 ± 0.2 (range 0.4 to 1.2). Only three patients (21 per cent) had a visual acuity less than 1.0. All patients with corneal conjunctivalisation used soft contact lenses, with a mean period of contact lens wear of 17.6 ± 8.5 years (CI 95%, 13 to 22, range six to 30). Two patients had used RGPs but at the time of diagnosis of corneal conjunctivalisation, all were using soft contact lens (15.2 years with a range from six to 30 years). We were unaware of specific characteristics of the previous contact lenses and solutions. All were daily contact lens wearers. Patients reported mean contact lens use of 12.5 ± 1.8 hours per day (CI 95%, 11.7 to 3.2). Only four (28 per cent, CI 95%, one to 35) of the patients reported previous ocular symptoms due to contact lenses wear. These symptoms were irritation (two patients), photophobia (two), red eye (two), dryness (one) or visual acuity decrease (one patient). The main clinical findings of cornea conjunctivalisation were irregular, hazy peripheral epithelial ingrowths of the corneal surface (Figures 1 and 2), superficial vascularisation (more than one cross), greater in the superior limbal area followed by the inferior area (Figure 1). The limbal regions of corneal conjunctivalisation showed a loss of limbal palisades of Vogt. Positive late fluorescein staining was reported in 43 per cent of eyes (CI 95%, 22.7 to 63) (Figure 3). Slitlamp examination showed bilateral corneal conjunctivalisation in 10 patients (71.4 per cent), corneal conjunctivalisation was superior in 79 per cent of eyes (CI 95%, 53 to 90) and inferior in only three eyes (12 per cent). The conjunctivalised area was bigger than the area of vascularisation (Figures 1 and 2). 27

silicone hydrogel and 14 per cent with RGP) and the remaining 21 per cent chose LASIK surgery.

3 Figure 1. Inferior conjunctivalisation with vascularisation Figure 2. Superior conjunctivalisation Discontinuation of contact lenses wear was proposed to 29 per cent of the patients, 50 per cent were fitting with high Dk contact lenses (36 per cent with disposable silicone hydrogel and 14 per cent with RGP) and the remaining 21 per cent chose LASIK surgery. DISCUSSION This study describes the clinical characteristics of the largest group of patients with corneal conjunctivalisation secondary to contact lens wear. These 14 patients were ascribed as contact lens-induced corneal conjunctivalisation after excluding all known aetiologies of LSCD (chemical or thermal burn, Stevens-Johnson syndrome, toxic epidermal necrolysis, multiple ocular surgeries, long-term topical medications, aniridia, coloboma, neoplasia, multiple hormonal deficiencies, peripheral ulcerative corneal diseases, neurotrophic keratopathy et cetera 1,2,5,6 ) except contact lens wear. 5 Contact lens wear is a well-known cause of corneal conjunctivalisation 1 3 but its prevalence, incidence and risk factors are unknown. Conjunctivalisation, vascularisation, pannus and mild keratitis were the main clinical findings of destruction or loss of limbal stem cells. 2 In contact lenses wearers, the differential diagnosis is proposed for disorders such as chronic corneal epitheliopathy, superior limbic keratoconjunctivitis, contact lens-induced keratoconjunctivitis (CLIK) and advancing wave-like epitheliopathy. 1,7 10 Lavker, Tseng and Sun 2 asserted that conjunctival epithelial ingrowth was the sine qua non criterion for LSCD diagnosis. Therefore, all patients diagnosed with corneal conjunctivalisation in this study should be in an initial stage of LSCD. The epithelial phenotype of the pannus in LSCD patients has negative staining to cornea specific anti-keratin monoclonal antibody (K3) and positive presence of conjunctival specific anti-keratin monoclonal antibody (K19) obtain by corneal impression cytology. 3,4 Nevertheless, corneal impression cytology is not a routine clinical procedure in contact lens practice. Donissi and colleagues, 4 concluded that impression cytology could have an important role in evaluating patients undergoing therapeutic penetrating keratoplasty to select those who would benefit from limbal stem cell transplantation. Impression cytology is essential to confirm if these patients have LSCD induced by contact lens wear. The aetiology of LSCD in contact lens wearers is uncertain. 1 There are many theories regarding its aetiology. Bloomfield, Jakobiec and Theodore 10 proposed that pannus occurs in response to a chronic irritation from contact lenses and/or solu- 28

4 Figure 3. Fluorescein staining over the vascularised corneal region with keratitis tion preservatives, such as thimerosol. Previous papers 9 found chronic corneal epitheliopathy occurred one to18 years after commencing soft contact lens wear in six patients with a history of exposure to thimerosol in contact lens solutions. All needed limbal transplantation. We found a mean of 17.6 years (range six to 30) of contact lens wear in our patients with corneal conjunctivalisation. All patients were cleaning their contact lenses with solutions without thimerosol, however, we are unable to ascertain if patients were ever exposed to thimerosol because the range of contact lenses wear was six to 30 years. None had used solutions with thimerosol in the few last years. If corneal conjunctivalisation was secondary to thimerosol exposure in early years of contact lens wear, these patients should have had more severe symptoms and signs because in contact lens wearers, LSCD proliferates and eventually grows onto the cornea if contact lens wear is not discontinued. 1 In our study, most patients (71.4 per cent) were asymptomatic. Another theory suggests that the cause may be mechanical pressure at the limbus from the superior eyelid and contact lens during blinking. 9 This theory does not explain patients with inferior corneal conjunctivalisation, as we found in two patients (14.3 per cent). The inferior limbus has minimal eyelid pressure but contact lenses can rub inferiorly. Hypoxia in contact lenses wearers can produce neovascularisation (pannus) from chronically tight lenses or excessive wearing of low oxygen permeable soft contact lenses. The traumatic theory cannot be discarded because of patients with LSCD secondary to ocular and/or systemic conditions and those associated with therapeutic soft contact lenses with low oxygen permeability and large diameter. 11 Therapeutic soft contact lenses eliminate the mechanical effects on the superior lid on the globe and protect the superior corneal limbus and adjacent bulbar conjunctiva. Initially, LSCD found in contact lens wearers affects the superior conjunctiva, 1 which proliferates and eventually grows onto the cornea if contact lens wear is continued. We found corneal conjunctivalisation in the inferior limbus in two patients. In all cases, the epithelium becomes diffusely thickened, opacified and often vascularised either superiorly or inferiorly. In addition, limbal palisades of Vogt are absent in slitlamp examination. Several authors 1 6 suggest that the symptoms of LSCD include severe photophobia and decreased vision if the visual axis is affected or if patients have moderate keratitis and recurrent corneal erosions. In our series, only four patients had these symptoms. Corneal conjunctivalisation may be subclinical or asymptomatic in the initial stages. 9 All cases of corneal conjunctivalisation occurred in soft contact lens wearers. The majority of practitioners fitted predominantly soft lenses, replaced monthly or more frequently. Ninety-three per cent of new fittings in Australia 12 were with soft lenses, of which seven per cent were for extended wear and of the refittings, 89 per cent were soft lenses and 18 per cent were extended wear. International Contact Lens Prescribing in a 2005 report (Contact Lens Spectrum, January 2006) showed similar proportions (90 per cent soft contact lenses versus 10 per cent rigid). Mid-water content with medium oxygen permeability was the most commonly used contact lens for daily wear and silicone hydrogel materials for extended wear. Moreover, 50 per cent of rigid lenses were prescribed using mid-dk materials. It is possible that prevalence and incidence of corneal conjunctivalisation in contact lens wearers will increase in the future. The demographic data confirmed that corneal conjunctivalisation occurs predominantly among females (93 per cent), which is similar to the findings reported in previous papers 13 on idiopathic LSCD. According to the International Contact Lens Prescribing in 2005 report, 60 to 70 per cent of contact lens wearers are women. 12 More research is necessary to determine if corneal conjunctivalisation or LSCD has a gender difference in longstanding contact lens wearers. Hypoxic and traumatic theories can explain corneal conjunctivalisation found in this series of patients. Both theories explain superior and inferior clinical signs. There is evidence that suggests the hypoxic theory because corneal pannus 14 and persistent corneal epithelial de- 29

5 fects 15,16 resolve with discontinuation of contact lens wear or with refitting using moderate to high oxygen permeable, rigid gas permeable or silicone hydrogel contact lenses. Optometrists who see large numbers of contact lens patients can play an important role in the initial diagnosis, education and management of corneal conjunctivalisation caused by contact lenses wear. This may involve suspension of contact lens wear, refitting with high oxygen permeability soft or RGP contact lenses or timely referral to a corneal specialist. CONCLUSIONS Long-standing contact lens wearers who develop corneal conjunctivalisation are predominantly female, asymptomatic and have been wearing daily disposable soft contact lenses for more than 10 hours per day wear, for six or more years. ACKNOWLEDGEMENTS I would like to thank Dr Agustin Mayo, IOBA and Department of Statistical and Operative Research, School of Science University of Valladolid, who provided statistical information for this study; Dr Herreras, Ocular Surface Group, IOBA Eye Institute for reviewing the paper; and Begoña Coco, IOBA, University of Valladolid, for checking the English of the manuscript. None of the authors has a financial or proprietary interest in any material or method mentioned. 5. Puangsricharern V, Tseng SC. Cytologic evidence of corneal diseases with limbal stem cell deficiency. Ophthalmology 1995; 102: Schwartz GS, Holland EJ. Iatrogenic limbal stem cell deficiency. Cornea 1998; 17: D Aversa G, Luchs JL, Fox MJ, Rosenbaum PS, Udell IJ. Advancing wave-like epitheliopathy. Clinical features and treatment. Ophthalmology 1997; 104: Robin SB, Epstein RJ, Kornmehl EW. Bandshaped, whorled microcystic cornea1 dystrophy. Am J Ophthalmol 1994; 117: Jenkins C, Tuft S, Liu C, Buckley R. Limbal transplantation in the management of chronic contact-lens-associated epitheliopathy. Eye 1993; 7: Bloomfield SE, Jakobiec FA, Theodore FH. Contact lens induced keratopathy: a severe complication extending the spectrum of keratoconjunctivitis in contact lens wearers. Ophthalmology 1984; 91: Mondino BJ, Zaidman GW, Salamon SW. Use of pressure patching and soft contact lenses in superior limbic keratoconjunctivitis. Arch Ophthalmol 1982; 100: Woods C, Morgan P. Contact lens prescribing in the Australian states and territories Clin Exp Optom 2002; 85: Espana E, Grueterich M, Romano A, Touhami A, Scheffer C, Tseng G. Idiopathic limbal stem cell deficiency. Ophthalmology 2002; 109: Chun M, Kageyama J. Corneal Pannus Resolved with silicone hydrogel contact lenses: A case series. ICLC 2000; 27: Rosenthal P, Cotter JM, Baum J. Treatment of persistent corneal epithelial defect with extended wear of a fluidventilated gas-permeable scleral contact lens. Am J Ophthalmol 2000; 130: Cotter JM, Rosenthal P, Baum J. Gas permeable scleral lenses in the management of non-healing corneal epithelial defects. Invest Ophthalmol Vis Sci 1997; 38: S137. REFERENCES 1. Achong R, Caroline P. Limbal stem cell deficiency in a contact lens-related case. Clin Eye Vis Care 1999; 11: Lavker R, Tseng S, Sun T. Corneal epithelial stem cells at the limbus: looking at some old problems from a new angle. Exp Eye Res 2003; 78: Espana E, Pascuale M, He H, Kawakita T, Raju V, Liu C, Tseng S. Characterization of corneal pannus removed from patients with total limbal stem cell deficiency. Invest Ophthalmol Vis Sci 2004; 45: Donisi PM, Rama P, Fasolo A, Ponzin D. Analysis of limbal stem cell deficiency by corneal impression cytology. Cornea 2003; 22: Corresponding author: Dr Raul Martin IOBA Eye Institute C/o Ramón y Cajal Valladolid SPAIN raul@ioba.med.uva.es 30

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