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Late-onset interface keratitis after uneventful laser in situ keratomileusis
Late-onset interface keratitis after uneventful laser in situ keratomileusis Louis E. Probst, MD, Linda Foley, OD ABSTRACT Although there have been many proposed etiologies for interface inflammation after laser in situ keratomileusis, the causative factor(s) remains an enigma. This case of late-onset interface inflammation suggests that the many previously suspected interface contaminants from the surgical environment were not involved. Transformation of a previously inert material to an inflammatory stimulus is proposed as a potential cause; however, a sample of inflammatory focus was not obtained because of the immediate and complete response to frequent topical steroid drops. J Cataract Refract Surg 2001; 27:1124 –1125 © 2001 ASCRS and ESCRS
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nterface keratitis after laser in situ keratomileusis (LASIK) typically occurs between 1 and 6 days after the LASIK procedure or manipulation of the corneal epithelium.1– 4 This is the first reported case of lateonset interface keratitis with no known stimulus 7 months after uneventful LASIK.
Case Report A healthy 30-year-old woman presented for correction of mild myopia at the TLC The Laser Eye Center–Madison. Preoperatively, best corrected visual acuity was 20/20 with – 4.25 – 0.50 ⫻ 170 in the right eye and 20/20 with – 4.75 – 0.50 ⫻ 5 in the left eye. The patient’s medical and family histories were unremarkable. The ocular history included daily-wear soft contact lenses for 19 years. Corneal thickness was 549 m in the right eye and 563 m in the left. Corneal topography was normal in both eyes. After informed consent was obtained, the patient had uneventful LASIK in both eyes with the VISX S2 laser and the Automated Corneal Shaper microkeratome with a 180 m plate. The target refraction was – 4.05 – 0.50 ⫻ 170 in the right eye and – 4.50 – 0.75 ⫻ 5 in the left eye. Povidone– Accepted for publication November 28, 2000. From TLC The Laser Eye Center–Madison, Madison, Wisconsin, USA. Reprint requests to Louis E. Probst, MD, Medical Director, TLC The Laser Eye Center–Madison, 2810 City View, Suite 200, Madison, Wisconsin 53718, USA. E-mail: louisprobst@hotmail. © 2001 ASCRS and ESCRS Published by Elsevier Science Inc.
iodine (Betadine威) was not used preoperatively. After the laser ablation, the flap was replaced and the interface was irrigated with a sterile balanced salt solution. There were no epithelial defects. The correct flap alignment was confirmed 20 minutes after the procedure. On the first postoperative day, the patient was comfortable with an uncorrected visual acuity (UCVA) of 20/20 in both eyes. The refraction was ⫹0.25 – 0.50 ⫻ 90 in the right eye and plano in the left eye. The corneal flaps were well positioned with smooth edges. The corneal interface was clear. The follow-up visits at 1 week and 1, 3, and 6 months were unremarkable with no significant change in refraction or UCVA. Seven months postoperatively, the patient presented with mild bulbar hyperemia, superior corneal pannus, and photophobia in the left eye. The UCVA was 20/20; however, a slitlamp examination showed interface inflammation in the superior one third of the flap extending from 12 to 3 o’clock. The inflammation consisted of visible microscopic white– gray opacities in the interface. The opacities were focused on a white spot located about 3.0 mm central from the flap edge. Inflammation radiated 2.0 mm from the center of an inflammatory area (Figure 1). The surface of the flap was normal. There was no anterior chamber reaction, and corneal topography was unremarkable. The patient was started on hourly prednisolone acetate 1% (Pred Forte威). Three days later, the interface inflammation had decreased by 80%, leaving a 1.0 mm inflammatory ring around the inflammatory focus. The topical steroid was tapered to 4 times a day for 1 week and then twice daily for 1 week. The follow-up examination immediately after cessation of the steroid drops found no evidence of interface inflammation or the 0886-3350/01/$–see front matter PII S0886-3350(01)00879-8
CASE REPORTS: PROBST
Figure 1. (Probst) Interface inflammation can be seen radiating from the white inflammatory focus in the interface at the edge of the pupil.
inflammatory focus. Uncorrected visual acuity remained 20/20 in the left eye.
Discussion Because the inflammation occurs in the interface, not in the lamellar flap itself, and the pattern of inflammation can be both diffuse and focal, the term LASIK interface keratitis more accurately describes this condition than diffuse lamellar keratitis or sands of the Sahara. Although the late onset and the focal nature of the interface keratitis were atypical, the case illustrates important variations in the syndrome that provide further insight into its pathogenesis. Previous reports describe LASIK interface keratitis as occurring between 1 and 6 days after the LASIK procedure.1–3 Manipulation of only the surface of the LASIK flap in another case resulted in an epithelial defect that resulted in interface keratitis.4 Because in our case there was no surgical manipulation of the cornea to provoke LASIK interface keratitis, corneal reaction to lamellar surgery can be eliminated as the causative factor. Also, the first 7 postoperative months were uneventful. Thus, the interface keratitis was unlikely a result of direct contamination from meibomian gland secretions, medication, surgical equipment, talc from surgical gloves, balanced salt solution, bacterial cell wall sensitivity, epithelial defects, lubricants from the microkeratome, or microkeratome blade debris, as previously
proposed (“Early Diagnosis of DLK, Topical Steroid Use Is Critical,” Ophthalmology Times, March 15, 2000, pages 32–33). Although LASIK interface keratitis has been described as diffuse and multifocal,1 this case demonstrated a single clear inflammatory focus in the interface, suggesting that this was the sole stimulus for the lateonset inflammation. Rather than a nonspecific reaction of the cornea to an unknown toxic or contaminating stimuli, the pattern of the inflammation suggests a single distinct cause of the interface keratitis. The relatively central location of the inflammatory focus in the interface rules out potential contamination after the procedure. The most probable cause of this focal inflammation is a localized reaction to staphylococcal exotoxin. The inflammatory cells produced by the exotoxin could have accumulated in the potential space created by the keratectomy. It is also possible that the inflammatory focus was introduced during the LASIK procedure but remained inert for 7 months. Perhaps some change, such as activation of a toxoplasma cyst or oxidation of a small metallic blade particle, occurred to this material to cause its transformation to an inflammatory stimulus. Because the patient responded well to frequent topical steroid treatment, there was no need to lift and irrigate under the flap. Therefore, no material was obtained for analysis. The causative factor of the LASIK interface keratitis in this case, as in most occurrences, remains an enigma.
References 1. Smith RJ, Maloney RK. Diffuse lamellar keratitis; a new syndrome in lamellar refractive surgery. Ophthalmology 1998; 105:1721–1726 2. Macaluso DC, Rich LF, MacRae S. Sterile interface keratitis after laser in situ keratomileusis: three episodes in one patient with concomitant contact dermatitis of the eyelids. J Refract Surg 1999; 15:679 – 682 3. MacRae S, Macaluso DC, Rich LF. Sterile interface keratitis associated with micropannus hemorrhage after laser in situ keratomileusis. J Cataract Refract Surg 1999; 25: 1679 –1681 4. Steinert RF, McColgin AZ, White A, Horsburgh GM. Diffuse interface keratitis after laser in situ keratomileusis (LASIK): a nonspecific syndrome. Am J Ophthalmol 2000; 129:380 –381
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I
nterface keratitis after laser in situ keratomileusis (LASIK) typically occurs between 1 and 6 days after the LASIK procedure or manipulation of the corneal epithelium.1– 4 This is the first reported case of lateonset interface keratitis with no known stimulus 7 months after uneventful LASIK.
Case Report A healthy 30-year-old woman presented for correction of mild myopia at the TLC The Laser Eye Center–Madison. Preoperatively, best corrected visual acuity was 20/20 with – 4.25 – 0.50 ⫻ 170 in the right eye and 20/20 with – 4.75 – 0.50 ⫻ 5 in the left eye. The patient’s medical and family histories were unremarkable. The ocular history included daily-wear soft contact lenses for 19 years. Corneal thickness was 549 m in the right eye and 563 m in the left. Corneal topography was normal in both eyes. After informed consent was obtained, the patient had uneventful LASIK in both eyes with the VISX S2 laser and the Automated Corneal Shaper microkeratome with a 180 m plate. The target refraction was – 4.05 – 0.50 ⫻ 170 in the right eye and – 4.50 – 0.75 ⫻ 5 in the left eye. Povidone– Accepted for publication November 28, 2000. From TLC The Laser Eye Center–Madison, Madison, Wisconsin, USA. Reprint requests to Louis E. Probst, MD, Medical Director, TLC The Laser Eye Center–Madison, 2810 City View, Suite 200, Madison, Wisconsin 53718, USA. E-mail: louisprobst@hotmail. © 2001 ASCRS and ESCRS Published by Elsevier Science Inc.
iodine (Betadine威) was not used preoperatively. After the laser ablation, the flap was replaced and the interface was irrigated with a sterile balanced salt solution. There were no epithelial defects. The correct flap alignment was confirmed 20 minutes after the procedure. On the first postoperative day, the patient was comfortable with an uncorrected visual acuity (UCVA) of 20/20 in both eyes. The refraction was ⫹0.25 – 0.50 ⫻ 90 in the right eye and plano in the left eye. The corneal flaps were well positioned with smooth edges. The corneal interface was clear. The follow-up visits at 1 week and 1, 3, and 6 months were unremarkable with no significant change in refraction or UCVA. Seven months postoperatively, the patient presented with mild bulbar hyperemia, superior corneal pannus, and photophobia in the left eye. The UCVA was 20/20; however, a slitlamp examination showed interface inflammation in the superior one third of the flap extending from 12 to 3 o’clock. The inflammation consisted of visible microscopic white– gray opacities in the interface. The opacities were focused on a white spot located about 3.0 mm central from the flap edge. Inflammation radiated 2.0 mm from the center of an inflammatory area (Figure 1). The surface of the flap was normal. There was no anterior chamber reaction, and corneal topography was unremarkable. The patient was started on hourly prednisolone acetate 1% (Pred Forte威). Three days later, the interface inflammation had decreased by 80%, leaving a 1.0 mm inflammatory ring around the inflammatory focus. The topical steroid was tapered to 4 times a day for 1 week and then twice daily for 1 week. The follow-up examination immediately after cessation of the steroid drops found no evidence of interface inflammation or the 0886-3350/01/$–see front matter PII S0886-3350(01)00879-8
CASE REPORTS: PROBST
Figure 1. (Probst) Interface inflammation can be seen radiating from the white inflammatory focus in the interface at the edge of the pupil.
inflammatory focus. Uncorrected visual acuity remained 20/20 in the left eye.
Discussion Because the inflammation occurs in the interface, not in the lamellar flap itself, and the pattern of inflammation can be both diffuse and focal, the term LASIK interface keratitis more accurately describes this condition than diffuse lamellar keratitis or sands of the Sahara. Although the late onset and the focal nature of the interface keratitis were atypical, the case illustrates important variations in the syndrome that provide further insight into its pathogenesis. Previous reports describe LASIK interface keratitis as occurring between 1 and 6 days after the LASIK procedure.1–3 Manipulation of only the surface of the LASIK flap in another case resulted in an epithelial defect that resulted in interface keratitis.4 Because in our case there was no surgical manipulation of the cornea to provoke LASIK interface keratitis, corneal reaction to lamellar surgery can be eliminated as the causative factor. Also, the first 7 postoperative months were uneventful. Thus, the interface keratitis was unlikely a result of direct contamination from meibomian gland secretions, medication, surgical equipment, talc from surgical gloves, balanced salt solution, bacterial cell wall sensitivity, epithelial defects, lubricants from the microkeratome, or microkeratome blade debris, as previously
proposed (“Early Diagnosis of DLK, Topical Steroid Use Is Critical,” Ophthalmology Times, March 15, 2000, pages 32–33). Although LASIK interface keratitis has been described as diffuse and multifocal,1 this case demonstrated a single clear inflammatory focus in the interface, suggesting that this was the sole stimulus for the lateonset inflammation. Rather than a nonspecific reaction of the cornea to an unknown toxic or contaminating stimuli, the pattern of the inflammation suggests a single distinct cause of the interface keratitis. The relatively central location of the inflammatory focus in the interface rules out potential contamination after the procedure. The most probable cause of this focal inflammation is a localized reaction to staphylococcal exotoxin. The inflammatory cells produced by the exotoxin could have accumulated in the potential space created by the keratectomy. It is also possible that the inflammatory focus was introduced during the LASIK procedure but remained inert for 7 months. Perhaps some change, such as activation of a toxoplasma cyst or oxidation of a small metallic blade particle, occurred to this material to cause its transformation to an inflammatory stimulus. Because the patient responded well to frequent topical steroid treatment, there was no need to lift and irrigate under the flap. Therefore, no material was obtained for analysis. The causative factor of the LASIK interface keratitis in this case, as in most occurrences, remains an enigma.
References 1. Smith RJ, Maloney RK. Diffuse lamellar keratitis; a new syndrome in lamellar refractive surgery. Ophthalmology 1998; 105:1721–1726 2. Macaluso DC, Rich LF, MacRae S. Sterile interface keratitis after laser in situ keratomileusis: three episodes in one patient with concomitant contact dermatitis of the eyelids. J Refract Surg 1999; 15:679 – 682 3. MacRae S, Macaluso DC, Rich LF. Sterile interface keratitis associated with micropannus hemorrhage after laser in situ keratomileusis. J Cataract Refract Surg 1999; 25: 1679 –1681 4. Steinert RF, McColgin AZ, White A, Horsburgh GM. Diffuse interface keratitis after laser in situ keratomileusis (LASIK): a nonspecific syndrome. Am J Ophthalmol 2000; 129:380 –381
J CATARACT REFRACT SURG—VOL 27, JULY 2001
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