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Haze after photorefractive keratectomy caused by iatrogenic lagophthalmos
J CATARACT REFRACT SURG - VOL 32, AUGUST 2006
Haze after photorefractive keratectomy caused by iatrogenic lagophthalmos Antonio Leccisotti, MD, PhD, Johnny Moore, FRCOphth, PhD
A 22-year-old man had shortening of the levator muscle for a congenital blepharoptosis in the right eye in 2000. In September 2004, he was successfully treated by bilateral photorefractive keratectomy (PRK) for myopia and was asymptomatic with an uncorrected visual acuity of 20/20. In October 2005, right eye visual acuity decreased because of an inferiorly localized haze caused by nocturnal lagophthalmos. Fluorometholone eyedrops and lubrication induced full visual recovery after 2 months, but corresponding topographical abnormalities were only partially improved. Corneal exposure can induce haze after PRK, even in the long term. The efficacy of topical steroids indicates a role for inflammatory mediators in this condition. Eyelid position and dynamics must be evaluated before PRK to rule out lagophthalmos. J Cataract Refract Surg 2006; 32:1392–1394 Q 2006 ASCRS and ESCRS
Lagophthalmos induces localized tear-film disturbances,1 and dry eye is a possible cause of haze after photorefractive keratectomy (PRK).2,3 However, the role of lagophthalmos in inducing haze has not been assessed (Medline search by http://www.pubmed.org; key words: photorefractive keratectomy, haze, dry eye, lagophthalmos, corneal exposure. Accessed December 20, 2005.). We report a case of localized corneal haze after PRK associated with corneal exposure due to previous blepharoptosis surgery. CASE REPORT In October 2005, a 23-year-old man was referred with reduced vision in his right eye. In 2000, the patient had had surgical repair of congenital blepharoptosis in the right eye by levator muscle resection. In September 2004, bilateral PRK had been performed elsewhere for the following ametropia: 4.00 1.00 130 in the right eye and 3.50 0.50 80 in the left eye. The postoperative course had been uneventful, and a bilateral uncorrected visual acuity (UCVA) of 20/20 had been achieved at 6 months. The patient had used lubricating eyedrops in the first
postoperative month and fluorometholone eyedrops 3 times daily in the first 4 months. On examination, the best corrected visual acuity (BCVA) in the right eye was 20/25 with 0.50 0.75 90 (20/20 with pinhole). At slitlamp, haze grade 1 was observed in the inferior half of the cornea (Figure 1). Tangential videokeratography revealed irregular steepening of the inferior cornea, corresponding to the hazy area of the cornea. Placido rings in the inferior cornea appeared interrupted and irregularly elongated in the central 3.0 mm (Figure 2). The UCVA in the left eye was 20/20, with no haze; videokeratography showed regular central flattening due to the previous myopic excimer ablation. In primary gaze position, the eyelid position appeared normal and symmetrical (Figure 3). In downgaze, the right superior eyelid remained 2.5 mm higher than the left (‘‘lid lag’’). The patient had not noticed any recent change in his eyelid position.
Accepted for publication February 20, 2006. From the Ophthalmic Surgery Unit (Leccisotti), Casa di Cura Rugani, Siena, Italy, and the Department of Ophthalmology RVH (Moore), Belfast, and the University of Ulster (Moore), Coleraine, Northern Ireland. Neither author has a financial or proprietary interest in any product or technique mentioned. Corresponding author: Antonio Leccisotti, MD, PhD, Piazza 5 Bersaglieri 2, 53100 Siena, Italy. E-mail: [email protected]. Q 2006 ASCRS and ESCRS Published by Elsevier Inc.
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Figure 1. Haze in the inferior half of the cornea induced by nocturnal lagophthalmos 1 year after myopic PRK (arrow, superior edge of haze). 0886-3350/06/$-see front matter doi:10.1016/j.jcrs.2006.02.080
CASE REPORTS: POST-PRK HAZE FROM IATROGENIC LAGOPHTHALMOS
Figure 2. Tangential videokeratography at presentation of inferior corneal haze, induced by nocturnal lagophthalmos. Irregular steepening of the inferior cornea.
Treatment in the right eye consisted of unpreserved fluorometholone 0.1% eyedrops 4 times daily, unpreserved sodium hyaluronate 0.2% eyedrops every 2 hours while awake, and a lubricating ointment (white petrolatum, lanolin, mineral oil) at bedtime. The parents of the patient were asked to record the eyelid position during sleep.
Two months later, at follow-up, the UCVA in the right eye was 20/20 and the inferior corneal haze reduced to 0.5. Tangential videokeratography showed almost regular Placido rings, and a reduced irregularity of the inferior cornea (Figure 4). The patient’s parents reported that during sleep the right cornea remained uncovered by approximately 1.0 mm. Fluorometholone eyedrops
Figure 3. Eyelid position in primary gaze (top) and downgaze (bottom). The right superior eyelid shows moderate lid retraction.
J CATARACT REFRACT SURG - VOL 32, AUGUST 2006
1393
CASE REPORTS: POST-PRK HAZE FROM IATROGENIC LAGOPHTHALMOS
Normal epithelial healing eliminates a large source of inflammatory cytokines, resulting in a controlled process of stromal remodeling and repair.10 The continued source of epithelial inflammation provoked by lagophthalmic corneal exposure may have been sufficient to induce epithelial hyperplasia and abnormal stromal repair.11 In our case, the use of steroids for 4 months after PRK may have delayed the inflammatory process, thus explaining the haze occurrence 1 year post PRK. The late onset of haze suggests that long-term lubrication is warranted in cases of corneal exposure in eyes to have PRK. In addition, the present case indicates that a thorough assessment of eyelid anamnesis, position, and movement are needed before PRK to rule out latent or subtle conditions of lagophthalmos. Figure 4. Tangential videokeratography 2 months after the image in Figure 2. Steroidal topical treatment and lubrication improved the Placido rings’ regularity. An uneven inferior corneal steepening persists.
were tapered, and nocturnal lubrication was continued indefinitely. DISCUSSION
In the present case, a causal relation between lagophthalmos and haze after PRK was evidenced by monocular occurrence and by localization in the area of nocturnal corneal exposure. To date, the pathogenesis of haze secondary to corneal exposure has not been highlighted in the literature. Corneal exposure results in ocular surface inflammation, characterized by a cocktail of inflammatory cytokines, growth factors, and infiltrating white blood cells.5–7 An initial effect of PRK in the anterior stroma is to induce apoptosis of anterior stromal keratocytes, which are subsequently replaced by repair-type keratocytes and myofibroblasts.4 These repair cells respond to inflammatory cytokines by expression of a milieu of other cytokines, chemokines, and growth factors designed to heal the cornea and remove any inciting inflammatory stimulus.8 Repair keratocytes are therefore responsive to autocrine and paracrine effects.9
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REFERENCES 1. Murube J, Ne´meth J, H} oh H. The triple classification of the dry eye for practical clinical use. Eur J Ophthalmol 2005; 15:660–667 2. Tervo T, Mustonen R, Tarkkanen A. Management of dry eye may reduce haze after excimer laser photorefractive keratectomy. Refract Corneal Surg 1993; 9:306 3. Corbett MC, O’Brart DP, Warburton FG, Marshall J. Biologic and environmental risk factors for regression after photorefractive keratectomy. Ophthalmology 1996; 03:1381–1391 4. Fantes FE, Hanna KD, Waring GO III, et al. Wound healing after excimer laser keratomileusis (photorefractive keratectomy) in monkeys. Arch Ophthalmol 1990; 108:665–675 5. Pflugfelder SC, Solomon A, Dursun D, Li DQ. Dry eye and delayed tear clearance: ‘‘a call to arms’’. Adv Exp Med Biol 2002; 506:739–743 6. Solomon A, Dursun D, Liu Z, et al. Pro- and anti-inflammatory forms of interleukin-1 in the tear fluid and conjunctiva of patients with dry-eye disease. Invest Ophthalmol Vis Sci 2001; 42:2283–2292 7. Barton K, Monroy D, Nava A, et al. Inflammatory cytokines in tears of patients with ocular rosacea. Ophthalmology 1997; 104:1868–1874 8. Wilson SE, Liu JJ, Mohan RR. Stromal-epithelial interactions in the cornea. Prog Retin Eye Res 1999; 18:293–309 9. Wilson SE, Mohan RR, Mohan RR, et al. The corneal wound healing response: cytokine-mediated interaction of the epithelium, stroma, and inflammatory cells. Prog Retin Eye Res 2001; 20:625–637 10. Wilson SE, Kim WJ. Keratocyte apoptosis: implications on corneal wound healing, tissue organization, and disease. Invest Ophthalmol Vis Sci 1998; 39:220–226 11. Nakamura K. Interaction between injured corneal epithelial cells and stromal cells. Cornea 2003; 22:S35–S47
J CATARACT REFRACT SURG - VOL 32, AUGUST 2006
Haze after photorefractive keratectomy caused by iatrogenic lagophthalmos Antonio Leccisotti, MD, PhD, Johnny Moore, FRCOphth, PhD
A 22-year-old man had shortening of the levator muscle for a congenital blepharoptosis in the right eye in 2000. In September 2004, he was successfully treated by bilateral photorefractive keratectomy (PRK) for myopia and was asymptomatic with an uncorrected visual acuity of 20/20. In October 2005, right eye visual acuity decreased because of an inferiorly localized haze caused by nocturnal lagophthalmos. Fluorometholone eyedrops and lubrication induced full visual recovery after 2 months, but corresponding topographical abnormalities were only partially improved. Corneal exposure can induce haze after PRK, even in the long term. The efficacy of topical steroids indicates a role for inflammatory mediators in this condition. Eyelid position and dynamics must be evaluated before PRK to rule out lagophthalmos. J Cataract Refract Surg 2006; 32:1392–1394 Q 2006 ASCRS and ESCRS
Lagophthalmos induces localized tear-film disturbances,1 and dry eye is a possible cause of haze after photorefractive keratectomy (PRK).2,3 However, the role of lagophthalmos in inducing haze has not been assessed (Medline search by http://www.pubmed.org; key words: photorefractive keratectomy, haze, dry eye, lagophthalmos, corneal exposure. Accessed December 20, 2005.). We report a case of localized corneal haze after PRK associated with corneal exposure due to previous blepharoptosis surgery. CASE REPORT In October 2005, a 23-year-old man was referred with reduced vision in his right eye. In 2000, the patient had had surgical repair of congenital blepharoptosis in the right eye by levator muscle resection. In September 2004, bilateral PRK had been performed elsewhere for the following ametropia: 4.00 1.00 130 in the right eye and 3.50 0.50 80 in the left eye. The postoperative course had been uneventful, and a bilateral uncorrected visual acuity (UCVA) of 20/20 had been achieved at 6 months. The patient had used lubricating eyedrops in the first
postoperative month and fluorometholone eyedrops 3 times daily in the first 4 months. On examination, the best corrected visual acuity (BCVA) in the right eye was 20/25 with 0.50 0.75 90 (20/20 with pinhole). At slitlamp, haze grade 1 was observed in the inferior half of the cornea (Figure 1). Tangential videokeratography revealed irregular steepening of the inferior cornea, corresponding to the hazy area of the cornea. Placido rings in the inferior cornea appeared interrupted and irregularly elongated in the central 3.0 mm (Figure 2). The UCVA in the left eye was 20/20, with no haze; videokeratography showed regular central flattening due to the previous myopic excimer ablation. In primary gaze position, the eyelid position appeared normal and symmetrical (Figure 3). In downgaze, the right superior eyelid remained 2.5 mm higher than the left (‘‘lid lag’’). The patient had not noticed any recent change in his eyelid position.
Accepted for publication February 20, 2006. From the Ophthalmic Surgery Unit (Leccisotti), Casa di Cura Rugani, Siena, Italy, and the Department of Ophthalmology RVH (Moore), Belfast, and the University of Ulster (Moore), Coleraine, Northern Ireland. Neither author has a financial or proprietary interest in any product or technique mentioned. Corresponding author: Antonio Leccisotti, MD, PhD, Piazza 5 Bersaglieri 2, 53100 Siena, Italy. E-mail: [email protected]. Q 2006 ASCRS and ESCRS Published by Elsevier Inc.
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Figure 1. Haze in the inferior half of the cornea induced by nocturnal lagophthalmos 1 year after myopic PRK (arrow, superior edge of haze). 0886-3350/06/$-see front matter doi:10.1016/j.jcrs.2006.02.080
CASE REPORTS: POST-PRK HAZE FROM IATROGENIC LAGOPHTHALMOS
Figure 2. Tangential videokeratography at presentation of inferior corneal haze, induced by nocturnal lagophthalmos. Irregular steepening of the inferior cornea.
Treatment in the right eye consisted of unpreserved fluorometholone 0.1% eyedrops 4 times daily, unpreserved sodium hyaluronate 0.2% eyedrops every 2 hours while awake, and a lubricating ointment (white petrolatum, lanolin, mineral oil) at bedtime. The parents of the patient were asked to record the eyelid position during sleep.
Two months later, at follow-up, the UCVA in the right eye was 20/20 and the inferior corneal haze reduced to 0.5. Tangential videokeratography showed almost regular Placido rings, and a reduced irregularity of the inferior cornea (Figure 4). The patient’s parents reported that during sleep the right cornea remained uncovered by approximately 1.0 mm. Fluorometholone eyedrops
Figure 3. Eyelid position in primary gaze (top) and downgaze (bottom). The right superior eyelid shows moderate lid retraction.
J CATARACT REFRACT SURG - VOL 32, AUGUST 2006
1393
CASE REPORTS: POST-PRK HAZE FROM IATROGENIC LAGOPHTHALMOS
Normal epithelial healing eliminates a large source of inflammatory cytokines, resulting in a controlled process of stromal remodeling and repair.10 The continued source of epithelial inflammation provoked by lagophthalmic corneal exposure may have been sufficient to induce epithelial hyperplasia and abnormal stromal repair.11 In our case, the use of steroids for 4 months after PRK may have delayed the inflammatory process, thus explaining the haze occurrence 1 year post PRK. The late onset of haze suggests that long-term lubrication is warranted in cases of corneal exposure in eyes to have PRK. In addition, the present case indicates that a thorough assessment of eyelid anamnesis, position, and movement are needed before PRK to rule out latent or subtle conditions of lagophthalmos. Figure 4. Tangential videokeratography 2 months after the image in Figure 2. Steroidal topical treatment and lubrication improved the Placido rings’ regularity. An uneven inferior corneal steepening persists.
were tapered, and nocturnal lubrication was continued indefinitely. DISCUSSION
In the present case, a causal relation between lagophthalmos and haze after PRK was evidenced by monocular occurrence and by localization in the area of nocturnal corneal exposure. To date, the pathogenesis of haze secondary to corneal exposure has not been highlighted in the literature. Corneal exposure results in ocular surface inflammation, characterized by a cocktail of inflammatory cytokines, growth factors, and infiltrating white blood cells.5–7 An initial effect of PRK in the anterior stroma is to induce apoptosis of anterior stromal keratocytes, which are subsequently replaced by repair-type keratocytes and myofibroblasts.4 These repair cells respond to inflammatory cytokines by expression of a milieu of other cytokines, chemokines, and growth factors designed to heal the cornea and remove any inciting inflammatory stimulus.8 Repair keratocytes are therefore responsive to autocrine and paracrine effects.9
1394
REFERENCES 1. Murube J, Ne´meth J, H} oh H. The triple classification of the dry eye for practical clinical use. Eur J Ophthalmol 2005; 15:660–667 2. Tervo T, Mustonen R, Tarkkanen A. Management of dry eye may reduce haze after excimer laser photorefractive keratectomy. Refract Corneal Surg 1993; 9:306 3. Corbett MC, O’Brart DP, Warburton FG, Marshall J. Biologic and environmental risk factors for regression after photorefractive keratectomy. Ophthalmology 1996; 03:1381–1391 4. Fantes FE, Hanna KD, Waring GO III, et al. Wound healing after excimer laser keratomileusis (photorefractive keratectomy) in monkeys. Arch Ophthalmol 1990; 108:665–675 5. Pflugfelder SC, Solomon A, Dursun D, Li DQ. Dry eye and delayed tear clearance: ‘‘a call to arms’’. Adv Exp Med Biol 2002; 506:739–743 6. Solomon A, Dursun D, Liu Z, et al. Pro- and anti-inflammatory forms of interleukin-1 in the tear fluid and conjunctiva of patients with dry-eye disease. Invest Ophthalmol Vis Sci 2001; 42:2283–2292 7. Barton K, Monroy D, Nava A, et al. Inflammatory cytokines in tears of patients with ocular rosacea. Ophthalmology 1997; 104:1868–1874 8. Wilson SE, Liu JJ, Mohan RR. Stromal-epithelial interactions in the cornea. Prog Retin Eye Res 1999; 18:293–309 9. Wilson SE, Mohan RR, Mohan RR, et al. The corneal wound healing response: cytokine-mediated interaction of the epithelium, stroma, and inflammatory cells. Prog Retin Eye Res 2001; 20:625–637 10. Wilson SE, Kim WJ. Keratocyte apoptosis: implications on corneal wound healing, tissue organization, and disease. Invest Ophthalmol Vis Sci 1998; 39:220–226 11. Nakamura K. Interaction between injured corneal epithelial cells and stromal cells. Cornea 2003; 22:S35–S47
J CATARACT REFRACT SURG - VOL 32, AUGUST 2006