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Corneal conjunctivalization management with high Dk RGP contact lenses
Contact Lens & Anterior Eye 32 (2009) 147–150
Contents lists available at ScienceDirect
Contact Lens & Anterior Eye journal homepage: www.elsevier.com/locate/clae
Short Communication
Corneal conjunctivalization management with high Dk RGP contact lenses Raul Martin * IOBA-Eye Institute and Department of Physics TAO – School of Optometry, University of Valladolid, Valladolid, Spain
A R T I C L E I N F O
A B S T R A C T
Keywords: Corneal conjunctivalization High Dk Contact lens Limbal stem cell deficiency
Purpose: To describe the management of corneal conjunctivalization with a high Dk RGP contact lens (CL) fitting. Methods: A high Dk RGP CL (Menicon Z-alpha Dk = 189, Japan) was fitted, after temporary suspension of CL wear (6 months and 3 weeks), in two patients (a 36-year-old female and a 38-year-old male) who had corneal conjunctivalization secondary to low Dk soft CL wear. Both patients had worn their soft CLs 12– 14 h per day without symptoms for the previous 18–20 years. Results: After 9–15 months of high Dk RGP wear, all signs of corneal conjunctivalization had disappeared (corneal vascularization, late fluorescein stain, etc.) and patients wore their RGP CL comfortably. Corneal conjunctivalization was resolved with non-invasive procedures (temporary discontinuation, preservative-free artificial tears and high Dk RGP CL fitting) and thus other treatments (topical or surgical treatments such as limbus transplantation, amniotic membrane transplant or others) were not necessary. Conclusions: Short temporary suspension of CL wear (3 weeks), preservative-free artificial tears and refitting with high oxygen permeability RGP CL may be an alternative for the management of corneal conjunctivalization secondary to CL wear. ß 2009 British Contact Lens Association. Published by Elsevier Ltd. All rights reserved.
1. Introduction There are many contact lens (CL)-related ocular surface disorders; one of the most important of these is corneal conjunctivalization [1,2]. Conjunctivalization and vascularization of the corneal surface are the most reliable clinical-diagnostic criteria for limbal stem cell deficiency (LSCD) [3–8]. LSCD may be subdivided into two major categories [5,6]. The first category includes limbal epithelial stem cell destruction by known or recognizable offenders such as a chemical or thermal burn, Stevens–Johnson syndrome/toxic epidermal necrosis, multiple ocular surgeries or long-term topical medications (iatrogenic) [9], severe microbial infection, radiation, and the use of antimetabolites including 5-fluorouracil and mitomycin C, as well as CL wear [1,2,5,6,10]. The second category is characterized by a gradual loss of the stem cell population without known or identifiable precipitating factors (aniridia and coloboma, neoplasia, multiple hormonal deficiencies, peripheral ulcerative corneal
* Correspondence address: IOBA-Eye Institute, University of Valladolid, Campus Miguel Delibes, Camino de cementerio s/n 47011, Valladolid, Spain. Tel.: +34 983 423559; fax: +34 983 423274. E-mail address: [email protected].
diseases, neurotrophic keratopathy and idiopathic limbal deficiency) [1,5,6,10]. Depending on the extent of limbal involvement, limbal deficiency may be classified as partial (localized or sectorial) or total (diffuse) [6–8]. In partial LSCD, some sectors of the limbal and corneal epithelium are normal. Also, LSCD may vary in severity from mild (abnormal epithelium covering a variable area of the cornea) to severe (when pupil area is affected) [6,7]. Other authors [8] scored LSCD according to cytology results (percentage of CK19 positive cells). Furthermore, LSCD may be asymptomatic or subclinical and then progress to severe conditions [6,7]. This paper presents two cases of asymptomatic corneal conjunctivalization secondary to CL wear in which high Dk RGP CLs were prescribed to correct the refractive ametropia and to manage conjunctivalization of the cornea. 2. Case report 1 A 36-year-old female patient had worn soft toric CLs (low water, HEMA material) for the past 20 years for 12 h a day. She reported that their CL was replaced every 2–3 years when attending a follow-up review. Her first visit to the IOBA Eye Institute was September, 2005. She was referred for a CL fitting with an ophthalmologist diagnosis of LSCD. She was asymptomatic
1367-0484/$ – see front matter ß 2009 British Contact Lens Association. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.clae.2008.12.005
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R. Martin / Contact Lens & Anterior Eye 32 (2009) 147–150
Fig. 1. Patient #1. Left (A) Superior limbus with corneal vascularization after 6 months of non-soft CL wear prior to RGP lens wear (first visit). Right (B) Same eye after 9 months of high Dk RGP wear with ghost-vessels in the superior limbus.
with her soft CLs, but at the time of the visit, she did not wear her CLs because she had a corneal ulcer 6 months prior. Her medical history and family medical history were unremarkable. Her best corrected visual acuity was 1.0 (6/6) in both eyes (OD 3.25 2.50 at 1808 and OS 3.50 3.50 at 1758). A slit lamp exam revealed corneal conjunctivalization in both eyes with diffuse corneal haze over the superior limbus. Also, 2.0 mm of corneal vascular ingrown (pannus) tissue in the superior cornea was detected in both eyes (Fig. 1A). Keratometry readings were OD 7.55/7.10 at 1808 and OS 7.60/7.00 at 1758 (without distortion). High Dk aspheric RGP CLs were fitted (OD back optic zone radius (BOZR) 7.60 mm, total diameter 9.60 mm and 3.00 D, VA 1.2 (6/5); OS BOZR 7.70 mm, total diameter 9.60 mm and 3.25 D, VA 1.2 (6/5)) manufactured with Z-alpha material (Dk = 189) by Menicon (Japan). After 9 months of wearing the high Dk RGP CLs, the patient returned to the clinic for follow-up. Visual acuity with RGP CLs was 1.2 (6/5) in both eyes. The slit lamp exam revealed normal ocular findings with ghost-vessels in the superior limbus in both eyes without conjunctivalization and fluorescein corneal staining (Fig. 1B).
+10.50 2.00 at 1758, VA 0.7 (6/9) and OS +10.75 1.75 108, VA 0.8 (6/7.5)). Visual acuity was improved in both eyes. Keratometry readings were OD 8.40/7.75 at 1708 and OS 8.25/7.85 at 108 (without distortion). High Dk aspheric RGP CLs were fitted (OD BOZR 8.35 mm, total diameter 9.60 mm and +12.50 D, VA 1.0 (6/6); OS BOZR 8.30 mm, total diameter 9.60 mm and +12.75 D, VA 0.9 (6/6.5)) that were manufactured with Z-alpha material (Dk = 189) by Menicon (Japan) (Fig. 3). After 15 months of high Dk RGP CL wear, the patient returned to the clinic to replace his CLs. Visual acuity with RGP CLs was 0.9 (6/ 6.5) in both eyes. A slit lamp exam revealed normal ocular findings in both eyes without corneal vascularization, conjunctivalization or fluorescein corneal staining (Fig. 2B).
3. Case report 2 A 38-year-old male patient had worn soft CLs (low water, HEMA material) for the past 18 years for 12–14 h per day. He cleaned his CLs with non-thimerosol multipurpose solution. His first visit to IOBA Eye Institute in May 2006 was a routine appointment to replace his CLs; he had no symptoms. His medical history and family medical history were unremarkable. Visual acuity with CLs was 0.4 (6/15) in both eyes. The slit lamp exam revealed corneal conjunctivalization in both eyes with diffuse corneal haze, with a triangular shaped fold of epithelium over the superior limbus. Also, bilateral superficial punctate keratitis with 2.0 mm of 3608 corneal vascular ingrowth was detected. Late fluorescein staining was documented after 10 min of fluorescein installation (Fig. 2A). The patient was diagnosed clinically with LSCD secondary to CL wear. 3 weeks of no CL wear with preservative-free artificial tears was prescribed (six times to day). After 3 weeks of not wearing CLs and after using artificial tears, the patient returned to the clinic for follow-up. Biomicroscopy showed a light corneal staining with late staining in the corneal conjunctivalization zone. The patient had high hyperopia (OD
Fig. 2. Patient #2. Superior (A) Localized conjunctivalization of the superior cornea with late fluorescein staining (first visit). Inferior (B) Superior limbus without corneal conjunctivalization or vascularization after 15 months of high Dk RGP CL wear.
R. Martin / Contact Lens & Anterior Eye 32 (2009) 147–150
Fig. 3. Fluorescein pattern of high Dk RGP CL fitting in patient #2 (left eye).
4. Discussion Contact lens wear is a known cause of LSCD [1,2,5,6,8]. Clinical presentation of LSCD involves conjunctivalization of the cornea (conjunctival epithelial ingrowths), corneal epithelium with a dull and irregular reflex, poor epithelialization (recurrent or persistent defects), corneal vascularization, loss of the palisades of Vogt, chronic stromal inflammation (keratitis mixed with scarring), ulceration, melting, perforation of the cornea and late fluorescein staining (positive staining of the corneal surface noted 10 min after instillation) [5,6,8,11]. Corneal conjunctivalization is the most reliable diagnostic sign of limbal deficiency [5,6]. However, definitive diagnosis is provided by the use of impression cytology [5,6,8,11]. Unfortunately, impression cytology is no longer a routine exploration in CL practice; this procedure is indicated in severe cases of LSCD [1–6]. Donisi et al. [8] found a 77% LSCD diagnosis confirmation with impression cytology in 13 CL wearers with corneal conjunctivalization. The differences between clinical (corneal conjunctivalization) and laboratory (impression cytology) diagnosis could be explained by the low quality of the impression, which does not permit the identification of the conjunctival cytokeratins (CK19) in the corneal surface [8]. Donisi et al. [8] reported only 41% of samples to possess a good or discrete quality impression and concluded that an improvement in the sampling method would produce more reliable results. The two cases represent clinical diagnoses (corneal conjunctivalization, corneal vascularization, late fluorescein staining, etc.) of partial asymptomatic LSCD (mainly localized in the superior limbus) secondary to soft CL wear [2–6]. The etiology of LSCD in CL wearers is uncertain [1,2]. There are three principal theories with regard to its etiology; chronic irritation from CL and/or solution preservatives, limbus mechanical pressure and hypoxia secondary to low Dk CL. Bloomfield proposed that pannus occurs in response to a chronic irritation from contact lenses and/or solution preservatives such as thimerosol [12]. Jenkins et al. [13] found chronic corneal epitheliopathy 1–18 years after commencing soft CL wear in six patients with a history of exposure to thimerosol in CL fluids. All needed limbal transplantation. Our patients had a history of 20 years of soft CL wear similar to other reports [2]. We are unable to report whether patients were ever exposed to thimerosol, because they began wearing CL approximately 20 years prior, but in recent years they cleaned their CL with nonthimerosol solutions. Limbus mechanical pressure from the superior eyelids and/or CL during blinking [1–13] and hypoxia [1–14] in CL wearers may
149
produce pannus, neovascularization or LSCD from chronically tight lenses or excessive hours per day spent wearing low oxygen permeability CL. Hypoxic and traumatic theories may explain corneal conjunctivalization found in these two patients. However, high Dk RGP lenses were fitted and corneal conjunctivalization was resolved. This result suggests that hypoxia may be more influential in the LSCD etiology of CL wearers [2–14], because RGP may cause mechanical trauma on the superior cornea through rubbing with the lid and CL [1]. Limbal transplantation (using autologous or homologous tissue), mechanical debridement of conjunctival epithelium from the corneal surface, amniotic membrane transplantation, penetrating keratoplasty, and immunosuppression therapy have been reported as treatments for LSCD [1,5,6]. In mild LSCD cases (partial or focal LSCD), preservative-free artificial tears and no CL wear for a long period of time have been prescribed with satisfactory results [1]. In case #1, CL wear was discontinued 6 months prior, but in case #2 we discontinued CL wear for 3 weeks with preservative-free artificial tears prior to fitting with high Dk RGP CLs. After 9 or 15 months of high Dk RGP CL wear, clinical signs of LSCD had disappeared (Figs. 1 and 2) in both cases. In LSCD secondary to CL wear, non-invasive treatment methods [1,5,6], such as discontinuation of CL wear (with preservative-free artificial tears) for a period of time (3 weeks in case #2) combined with high Dk CL refitting may be an alternative for LSCD management. If cases do not resolve or LSCD progresses, definitive discontinuation of CL wear and referral of patients to corneal specialists are indicated. Achong and Caroline [1] concluded that less invasive treatment (lubricant therapy without CL wear) may need to be longer (6 months). In case #1, 6 months of discontinuation and 9 months of high Dk CL wear were necessary to resolve the corneal conjunctivalization. In case #2, we only discontinued CL wear for 3 weeks, but 15 months of high Dk CL wear was necessary for the resolution of the corneal conjunctivalization. These results suggest that a long period of CL discontinuation could be unnecessary if high Dk CLs are prescribed for partial LSCD. However, long periods of time might be necessary for corneal conjunctivalization to disappear. Contact lens wear has a wide range of therapeutic applications. It may be used to protect injured or diseased tissue, and to aid the return to a normal anatomical and functional state [15]. In the two cases reported here, RGP high Dk CL helped to return corneal epithelial stem cells, located in the limbus, to normal function. Patients have better VA with CL than with the VA provided with spectacles (moderate astigmatism and high hyperopia). This is the first report of the therapeutic use of RGP CL in LSCD management. Optometrists who see a large number of CL patients have an important role in the early diagnosis, education, management (temporary suspension of CL wear, preservative-free artificial tears, refitting with high oxygen permeability CL) or timely referral of cases of corneal conjunctivalization (LSCD) caused by CL wear. 5. Conclusion Short-term suspension of CL wear, preservative-free artificial tears and refitting with high oxygen permeability RGP CLs might be an alternative management tool for corneal conjunctivalization (LSCD) secondary to CL wear. Conflict of interest statement The author has no proprietary, financial or commercial interest in any material or method mentioned in this study.
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R. Martin / Contact Lens & Anterior Eye 32 (2009) 147–150
References [1] Achong R, Caroline P. Limbal stem cell deficiency in a contact lens-related case. Clin Eye Vision Care 1999;11:191–7. [2] Martin R. Corneal conjunctivalization in long standing contact lenses wearers. Clin Exp Optom 2007;90(1):26–30. [3] Patel NP, Kim T, Rapuano CJ, Cohen EJ, Laibson PR. Indications for and outcomes of repeat penetrating keratoplasty, 1989–1995. Ophthalmology 2000;107:719L 24. [4] Uchino Y, Goto E, Takano Y, Dogru M, Shinozaki N, Shimmura S, et al. Longstanding bullous keratopathy is associated with peripheral conjunctivalization and limbal deficiency. Ophthalmology 2006;113:1098–101. [5] Lavker RM, Tsengb SC, Sun TT. Corneal epithelial stem cells at the limbus: looking at some old problems from a new angle. Exp Eye Res 2004;78:433–46. [6] Dua HS, Azuara-Blanco A. Limbal stem cells of the corneal epithelium. Surv Ophthalmol 2000;44:415–25. [7] Dua HS, Joseph A, Shanmuganathan VA, Jones RE. Stem cell differentiation and the effects of deficiency. Eye 2003;17:877–85.
[8] Donisi PM, Rama P, Fasolo A, Ponzin D. Analysis of limbal stem cell deficiency by corneal impression cytology. Cornea 2003;22:533–8. [9] Schwartz GS, Holland EJ. Iatrogenic limbal stem cell deficiency. Cornea 1998;17:31–7. [10] Puangsricharern V, Tseng SC. Cytologic evidence of corneal diseases with limbal stem cell deficiency. Ophthalmology 1995;102:1476–85. [11] Espana EM, Grueterich M, Romano AC, Touhami A, Tseng SC. Idiopathic limbal stem cell deficiency. Ophthalmology 2002;109:2004–10. [12] Bloomfield SE, Jakobiec FA, Theodore FH. Contact lens induced keratopathy: a severe complication extending the spectrum of keratoconjunctivitis in contact lens wearers. Ophthalmology 1984;91:290–4. [13] Jenkins C, Tuft S, Liu C, Buckley R. Limbal transplantation in the management of chronic contact-lens-associated epitheliopathy. Eye 1993;7: 629–33. [14] Chun M, Kageyama J. Corneal pannus resolved with silicone hydrogel contact lenses: a case series. ICLC 2000;27:170–3. [15] Rubinstein MP. Applications of contact lens devices in the management of corneal disease. Eye 2003;17:872–6.
Contents lists available at ScienceDirect
Contact Lens & Anterior Eye journal homepage: www.elsevier.com/locate/clae
Short Communication
Corneal conjunctivalization management with high Dk RGP contact lenses Raul Martin * IOBA-Eye Institute and Department of Physics TAO – School of Optometry, University of Valladolid, Valladolid, Spain
A R T I C L E I N F O
A B S T R A C T
Keywords: Corneal conjunctivalization High Dk Contact lens Limbal stem cell deficiency
Purpose: To describe the management of corneal conjunctivalization with a high Dk RGP contact lens (CL) fitting. Methods: A high Dk RGP CL (Menicon Z-alpha Dk = 189, Japan) was fitted, after temporary suspension of CL wear (6 months and 3 weeks), in two patients (a 36-year-old female and a 38-year-old male) who had corneal conjunctivalization secondary to low Dk soft CL wear. Both patients had worn their soft CLs 12– 14 h per day without symptoms for the previous 18–20 years. Results: After 9–15 months of high Dk RGP wear, all signs of corneal conjunctivalization had disappeared (corneal vascularization, late fluorescein stain, etc.) and patients wore their RGP CL comfortably. Corneal conjunctivalization was resolved with non-invasive procedures (temporary discontinuation, preservative-free artificial tears and high Dk RGP CL fitting) and thus other treatments (topical or surgical treatments such as limbus transplantation, amniotic membrane transplant or others) were not necessary. Conclusions: Short temporary suspension of CL wear (3 weeks), preservative-free artificial tears and refitting with high oxygen permeability RGP CL may be an alternative for the management of corneal conjunctivalization secondary to CL wear. ß 2009 British Contact Lens Association. Published by Elsevier Ltd. All rights reserved.
1. Introduction There are many contact lens (CL)-related ocular surface disorders; one of the most important of these is corneal conjunctivalization [1,2]. Conjunctivalization and vascularization of the corneal surface are the most reliable clinical-diagnostic criteria for limbal stem cell deficiency (LSCD) [3–8]. LSCD may be subdivided into two major categories [5,6]. The first category includes limbal epithelial stem cell destruction by known or recognizable offenders such as a chemical or thermal burn, Stevens–Johnson syndrome/toxic epidermal necrosis, multiple ocular surgeries or long-term topical medications (iatrogenic) [9], severe microbial infection, radiation, and the use of antimetabolites including 5-fluorouracil and mitomycin C, as well as CL wear [1,2,5,6,10]. The second category is characterized by a gradual loss of the stem cell population without known or identifiable precipitating factors (aniridia and coloboma, neoplasia, multiple hormonal deficiencies, peripheral ulcerative corneal
* Correspondence address: IOBA-Eye Institute, University of Valladolid, Campus Miguel Delibes, Camino de cementerio s/n 47011, Valladolid, Spain. Tel.: +34 983 423559; fax: +34 983 423274. E-mail address: [email protected].
diseases, neurotrophic keratopathy and idiopathic limbal deficiency) [1,5,6,10]. Depending on the extent of limbal involvement, limbal deficiency may be classified as partial (localized or sectorial) or total (diffuse) [6–8]. In partial LSCD, some sectors of the limbal and corneal epithelium are normal. Also, LSCD may vary in severity from mild (abnormal epithelium covering a variable area of the cornea) to severe (when pupil area is affected) [6,7]. Other authors [8] scored LSCD according to cytology results (percentage of CK19 positive cells). Furthermore, LSCD may be asymptomatic or subclinical and then progress to severe conditions [6,7]. This paper presents two cases of asymptomatic corneal conjunctivalization secondary to CL wear in which high Dk RGP CLs were prescribed to correct the refractive ametropia and to manage conjunctivalization of the cornea. 2. Case report 1 A 36-year-old female patient had worn soft toric CLs (low water, HEMA material) for the past 20 years for 12 h a day. She reported that their CL was replaced every 2–3 years when attending a follow-up review. Her first visit to the IOBA Eye Institute was September, 2005. She was referred for a CL fitting with an ophthalmologist diagnosis of LSCD. She was asymptomatic
1367-0484/$ – see front matter ß 2009 British Contact Lens Association. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.clae.2008.12.005
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R. Martin / Contact Lens & Anterior Eye 32 (2009) 147–150
Fig. 1. Patient #1. Left (A) Superior limbus with corneal vascularization after 6 months of non-soft CL wear prior to RGP lens wear (first visit). Right (B) Same eye after 9 months of high Dk RGP wear with ghost-vessels in the superior limbus.
with her soft CLs, but at the time of the visit, she did not wear her CLs because she had a corneal ulcer 6 months prior. Her medical history and family medical history were unremarkable. Her best corrected visual acuity was 1.0 (6/6) in both eyes (OD 3.25 2.50 at 1808 and OS 3.50 3.50 at 1758). A slit lamp exam revealed corneal conjunctivalization in both eyes with diffuse corneal haze over the superior limbus. Also, 2.0 mm of corneal vascular ingrown (pannus) tissue in the superior cornea was detected in both eyes (Fig. 1A). Keratometry readings were OD 7.55/7.10 at 1808 and OS 7.60/7.00 at 1758 (without distortion). High Dk aspheric RGP CLs were fitted (OD back optic zone radius (BOZR) 7.60 mm, total diameter 9.60 mm and 3.00 D, VA 1.2 (6/5); OS BOZR 7.70 mm, total diameter 9.60 mm and 3.25 D, VA 1.2 (6/5)) manufactured with Z-alpha material (Dk = 189) by Menicon (Japan). After 9 months of wearing the high Dk RGP CLs, the patient returned to the clinic for follow-up. Visual acuity with RGP CLs was 1.2 (6/5) in both eyes. The slit lamp exam revealed normal ocular findings with ghost-vessels in the superior limbus in both eyes without conjunctivalization and fluorescein corneal staining (Fig. 1B).
+10.50 2.00 at 1758, VA 0.7 (6/9) and OS +10.75 1.75 108, VA 0.8 (6/7.5)). Visual acuity was improved in both eyes. Keratometry readings were OD 8.40/7.75 at 1708 and OS 8.25/7.85 at 108 (without distortion). High Dk aspheric RGP CLs were fitted (OD BOZR 8.35 mm, total diameter 9.60 mm and +12.50 D, VA 1.0 (6/6); OS BOZR 8.30 mm, total diameter 9.60 mm and +12.75 D, VA 0.9 (6/6.5)) that were manufactured with Z-alpha material (Dk = 189) by Menicon (Japan) (Fig. 3). After 15 months of high Dk RGP CL wear, the patient returned to the clinic to replace his CLs. Visual acuity with RGP CLs was 0.9 (6/ 6.5) in both eyes. A slit lamp exam revealed normal ocular findings in both eyes without corneal vascularization, conjunctivalization or fluorescein corneal staining (Fig. 2B).
3. Case report 2 A 38-year-old male patient had worn soft CLs (low water, HEMA material) for the past 18 years for 12–14 h per day. He cleaned his CLs with non-thimerosol multipurpose solution. His first visit to IOBA Eye Institute in May 2006 was a routine appointment to replace his CLs; he had no symptoms. His medical history and family medical history were unremarkable. Visual acuity with CLs was 0.4 (6/15) in both eyes. The slit lamp exam revealed corneal conjunctivalization in both eyes with diffuse corneal haze, with a triangular shaped fold of epithelium over the superior limbus. Also, bilateral superficial punctate keratitis with 2.0 mm of 3608 corneal vascular ingrowth was detected. Late fluorescein staining was documented after 10 min of fluorescein installation (Fig. 2A). The patient was diagnosed clinically with LSCD secondary to CL wear. 3 weeks of no CL wear with preservative-free artificial tears was prescribed (six times to day). After 3 weeks of not wearing CLs and after using artificial tears, the patient returned to the clinic for follow-up. Biomicroscopy showed a light corneal staining with late staining in the corneal conjunctivalization zone. The patient had high hyperopia (OD
Fig. 2. Patient #2. Superior (A) Localized conjunctivalization of the superior cornea with late fluorescein staining (first visit). Inferior (B) Superior limbus without corneal conjunctivalization or vascularization after 15 months of high Dk RGP CL wear.
R. Martin / Contact Lens & Anterior Eye 32 (2009) 147–150
Fig. 3. Fluorescein pattern of high Dk RGP CL fitting in patient #2 (left eye).
4. Discussion Contact lens wear is a known cause of LSCD [1,2,5,6,8]. Clinical presentation of LSCD involves conjunctivalization of the cornea (conjunctival epithelial ingrowths), corneal epithelium with a dull and irregular reflex, poor epithelialization (recurrent or persistent defects), corneal vascularization, loss of the palisades of Vogt, chronic stromal inflammation (keratitis mixed with scarring), ulceration, melting, perforation of the cornea and late fluorescein staining (positive staining of the corneal surface noted 10 min after instillation) [5,6,8,11]. Corneal conjunctivalization is the most reliable diagnostic sign of limbal deficiency [5,6]. However, definitive diagnosis is provided by the use of impression cytology [5,6,8,11]. Unfortunately, impression cytology is no longer a routine exploration in CL practice; this procedure is indicated in severe cases of LSCD [1–6]. Donisi et al. [8] found a 77% LSCD diagnosis confirmation with impression cytology in 13 CL wearers with corneal conjunctivalization. The differences between clinical (corneal conjunctivalization) and laboratory (impression cytology) diagnosis could be explained by the low quality of the impression, which does not permit the identification of the conjunctival cytokeratins (CK19) in the corneal surface [8]. Donisi et al. [8] reported only 41% of samples to possess a good or discrete quality impression and concluded that an improvement in the sampling method would produce more reliable results. The two cases represent clinical diagnoses (corneal conjunctivalization, corneal vascularization, late fluorescein staining, etc.) of partial asymptomatic LSCD (mainly localized in the superior limbus) secondary to soft CL wear [2–6]. The etiology of LSCD in CL wearers is uncertain [1,2]. There are three principal theories with regard to its etiology; chronic irritation from CL and/or solution preservatives, limbus mechanical pressure and hypoxia secondary to low Dk CL. Bloomfield proposed that pannus occurs in response to a chronic irritation from contact lenses and/or solution preservatives such as thimerosol [12]. Jenkins et al. [13] found chronic corneal epitheliopathy 1–18 years after commencing soft CL wear in six patients with a history of exposure to thimerosol in CL fluids. All needed limbal transplantation. Our patients had a history of 20 years of soft CL wear similar to other reports [2]. We are unable to report whether patients were ever exposed to thimerosol, because they began wearing CL approximately 20 years prior, but in recent years they cleaned their CL with nonthimerosol solutions. Limbus mechanical pressure from the superior eyelids and/or CL during blinking [1–13] and hypoxia [1–14] in CL wearers may
149
produce pannus, neovascularization or LSCD from chronically tight lenses or excessive hours per day spent wearing low oxygen permeability CL. Hypoxic and traumatic theories may explain corneal conjunctivalization found in these two patients. However, high Dk RGP lenses were fitted and corneal conjunctivalization was resolved. This result suggests that hypoxia may be more influential in the LSCD etiology of CL wearers [2–14], because RGP may cause mechanical trauma on the superior cornea through rubbing with the lid and CL [1]. Limbal transplantation (using autologous or homologous tissue), mechanical debridement of conjunctival epithelium from the corneal surface, amniotic membrane transplantation, penetrating keratoplasty, and immunosuppression therapy have been reported as treatments for LSCD [1,5,6]. In mild LSCD cases (partial or focal LSCD), preservative-free artificial tears and no CL wear for a long period of time have been prescribed with satisfactory results [1]. In case #1, CL wear was discontinued 6 months prior, but in case #2 we discontinued CL wear for 3 weeks with preservative-free artificial tears prior to fitting with high Dk RGP CLs. After 9 or 15 months of high Dk RGP CL wear, clinical signs of LSCD had disappeared (Figs. 1 and 2) in both cases. In LSCD secondary to CL wear, non-invasive treatment methods [1,5,6], such as discontinuation of CL wear (with preservative-free artificial tears) for a period of time (3 weeks in case #2) combined with high Dk CL refitting may be an alternative for LSCD management. If cases do not resolve or LSCD progresses, definitive discontinuation of CL wear and referral of patients to corneal specialists are indicated. Achong and Caroline [1] concluded that less invasive treatment (lubricant therapy without CL wear) may need to be longer (6 months). In case #1, 6 months of discontinuation and 9 months of high Dk CL wear were necessary to resolve the corneal conjunctivalization. In case #2, we only discontinued CL wear for 3 weeks, but 15 months of high Dk CL wear was necessary for the resolution of the corneal conjunctivalization. These results suggest that a long period of CL discontinuation could be unnecessary if high Dk CLs are prescribed for partial LSCD. However, long periods of time might be necessary for corneal conjunctivalization to disappear. Contact lens wear has a wide range of therapeutic applications. It may be used to protect injured or diseased tissue, and to aid the return to a normal anatomical and functional state [15]. In the two cases reported here, RGP high Dk CL helped to return corneal epithelial stem cells, located in the limbus, to normal function. Patients have better VA with CL than with the VA provided with spectacles (moderate astigmatism and high hyperopia). This is the first report of the therapeutic use of RGP CL in LSCD management. Optometrists who see a large number of CL patients have an important role in the early diagnosis, education, management (temporary suspension of CL wear, preservative-free artificial tears, refitting with high oxygen permeability CL) or timely referral of cases of corneal conjunctivalization (LSCD) caused by CL wear. 5. Conclusion Short-term suspension of CL wear, preservative-free artificial tears and refitting with high oxygen permeability RGP CLs might be an alternative management tool for corneal conjunctivalization (LSCD) secondary to CL wear. Conflict of interest statement The author has no proprietary, financial or commercial interest in any material or method mentioned in this study.
150
R. Martin / Contact Lens & Anterior Eye 32 (2009) 147–150
References [1] Achong R, Caroline P. Limbal stem cell deficiency in a contact lens-related case. Clin Eye Vision Care 1999;11:191–7. [2] Martin R. Corneal conjunctivalization in long standing contact lenses wearers. Clin Exp Optom 2007;90(1):26–30. [3] Patel NP, Kim T, Rapuano CJ, Cohen EJ, Laibson PR. Indications for and outcomes of repeat penetrating keratoplasty, 1989–1995. Ophthalmology 2000;107:719L 24. [4] Uchino Y, Goto E, Takano Y, Dogru M, Shinozaki N, Shimmura S, et al. Longstanding bullous keratopathy is associated with peripheral conjunctivalization and limbal deficiency. Ophthalmology 2006;113:1098–101. [5] Lavker RM, Tsengb SC, Sun TT. Corneal epithelial stem cells at the limbus: looking at some old problems from a new angle. Exp Eye Res 2004;78:433–46. [6] Dua HS, Azuara-Blanco A. Limbal stem cells of the corneal epithelium. Surv Ophthalmol 2000;44:415–25. [7] Dua HS, Joseph A, Shanmuganathan VA, Jones RE. Stem cell differentiation and the effects of deficiency. Eye 2003;17:877–85.
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