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Steroid-Induced Glaucoma After Laser in Situ Keratomileusis Associated with Interface Fluid

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Steroid-Induced Glaucoma After Laser in Situ Keratomileusis Associated with Interface Fluid Steroid-induced Glaucoma after Laser In Situ Keratomileusis Associated with Interface Fluid David Rex Hamilton, MD, MS,1 Edward E. Manche, MD,2 Larry F. Rich, MD,3 Robert K. Maloney, MD, MA (Oxon)4 Purpose: To report the ocular manifestations and clinical course of eyes developing interface fluid after laser in situ keratomileusis (LASIK) surgery from a steroid-induced rise in intraocular pressure. Design: Retrospective, noncomparative interventional case series. Participants/Intervention: We examined six eyes of four patients who had diffuse lamellar keratitis develop after uneventful myopic LASIK surgery and were treated with topical corticosteroids. Principal Outcome Measure: Slit-lamp findings, intraocular pressure measurements, and visual field loss. Results: All eyes had a pocket of fluid develop in the lamellar interface between the flap and the stromal bed associated with a corticosteroid-induced rise in intraocular pressure. However, because of the interface fluid, intraocular pressure was normal or low by central corneal Goldmann applanation tonometry in all eyes. The elevated intraocular pressure was diagnosed by peripheral measurement in several cases after months of elevated pressure. All six eyes had visual field defects develop. Three eyes of two patients had severe glaucomatous optic neuropathy and decreased visual acuity develop as a result of undiagnosed steroid-induced elevated intraocular pressure. Conclusions: A steroid-induced rise in intraocular pressure after LASIK can cause transudation of aqueous fluid across the endothelium that collects in the flap interface. The interface fluid leads to inaccurately low central applanation tonometry measurements that obscure the diagnosis of steroid-induced glaucoma. Serious visual loss may result. Ophthalmology 2002;109:659–665 © 2002 by the American Academy of Ophthalmology. The first report of interface fluid developing after laser in Fluid collected in the potential space between the flap and situ keratomileusis (LASIK) was reported by Lyle and Jin.1 bed, causing erroneous applanation tonometry readings. Re- This case featured steroid-induced intraocular pressure ele- cently, Rehany et al3 and Protellinha et al4 reported similar vation and falsely low intraocular pressure reading from cases. Since our first report (Case 1), we have collected applanation tonometry. The pocket of interface fluid, how- three additional cases of fluid developing between the epi- ever, was believed to be related to the presence of epithelial thelial flap and stromal bed after LASIK in eyes treated with ingrowth. Subsequently, we reported a case of interface topical steroids for diffuse lamellar keratitis. In these cases, fluid after LASIK surgery in a patient with diffuse lamellar intraocular pressure measured by applanation tonometry keratitis without epithelial ingrowth who went on to have suggested hypotony because of the collection of interface severe optic neuropathy develop from steroid-induced ele- fluid. We believe this complication warrants early recogni- vated glaucoma.2 We hypothesized that the fluid resulted tion and special attention to intraocular pressure measure- from transudation of aqueous across the stromal bed, result- ment to avoid potentially devastating vision loss. ing from steroid-induced elevated intraocular pressure. Case Reports Originally received: May 24, 2001. Accepted: September 19, 2001. Manuscript no. 210349. 1 Jules Stein Eye Institute, University of California, Los Angeles, Califor- Case 1 nia. A 58-year-old man was referred to us in consultation after having 2 Department of Ophthalmology, Stanford Hospital and Clinics, Palo Alto, undergone bilateral LASIK 6 months previously. The patient’s California. preoperative cycloplegic refraction was Ϫ10.00 Ϫ0.25 ϫ 110 in 3 Casey Eye Institute, Oregon Health Sciences University, Portland, Ore- the right eye and Ϫ8.25 Ϫ1.50 ϫ 140 in the left eye with gon. best-corrected visual acuity of 20/20 in each eye. Preoperative 4 Maloney-Seibel Vision Institute, Los Angeles, California. intraocular pressure was 18 mmHg by applanation in both eyes. Presented in part at the annual meeting of the American Academy of Funduscopic examination revealed pink optic nerves with cup-to- Ophthalmology, New Orleans, Louisiana, November 2001. disc ratios of 0.4 in the right eye and 0.5 in the left eye. There was Reprint requests to Robert K. Maloney, MD, MA (Oxon), Maloney-Seibel no prior history of glaucoma. Preoperative keratometry showed Vision Institute, 10921 Wilshire Boulevard, Suite 900, Los Angeles, Cal- corneal curvatures of 44.50/44.50 in the right eye and 43.62/ ifornia 90024. 44.37 ϫ 062 in the left eye. Corneal pachymetry was 575 ␮min © 2002 by the American Academy of Ophthalmology ISSN 0161-6420/02/$–see front matter 659 Published by Elsevier Science Inc. PII S0161-6420(01)01023-5 Ophthalmology Volume 109, Number 4, April 2002 the right eye and 569 ␮m in the left eye. The procedure consisted of creating a 160-␮m thick flap with a 6.0-mm ablation zone of 96 ␮m in central depth in the right eye and 76 ␮m in central depth in the left eye, leaving residual stromal beds of 319 ␮m in the right eye and 333 ␮m in the left eye. The patient reported mild, intermittent discomfort in the left eye at the postoperative week 3 visit. The left eye was diagnosed with mild diffuse lamellar keratitis, characterized by diffuse gran- ular haze in the interface, reducing uncorrected visual acuity to 20/200. The patient was started on fluorometholone acetate 0.1% (Flarex, Alcon Laboratories, Ft. Worth, TX) four times daily in the left eye. Vision decreased to the 20/400 to count fingers range by postoperative month 2. Keratometry readings were 41.50/37.75 ϫ 115 in the left eye. The cornea revealed diffuse haze in the flap with microcystic edema at the edge. Intraocular pressure by ap- planation was 12 mmHg. The patient was started on prednisolone acetate 1% (Pred Forte, Allergan, Irvine, CA) four times daily but increased to every 2 hours 2 weeks later when there were no signs of improvement. At the 4-month postoperative visit, uncorrected visual acuity remained at 20/400 in the left eye with 2ϩ micro- cystic edema, and intraocular pressure was 7 mmHg by applana- tion. Topical steroids were increased to every hour in the left eye. One week later, pressure was found to be 25 mmHg by Kowa portable applanation tonometer (Kowa Co., Ltd., Tokyo, Japan) in the left eye. Steroids were reduced to four times daily, and bet- Figure 1. Case 1, right eye. Visual field 7 months after laser in situ axolol hydrochloride, 0.25% (Betoptic-S, Alcon Laboratories, Ft. keratomileusis surgery. There is a suggestion of early superior and inferior Worth, TX) was started. At the 5-month postoperative visit, un- arcuate defects. The left eye could not undergo visual field testing because corrected visual acuity was 20/20 in the right eye and count fingers of light perception visual acuity. at 1 foot in the left eye with a 0.9 cup-to-disc ratio and a pressure of 10 mmHg by applanation tonometry. The patient was referred for consultation. corrected visual acuity of 20/30 in each eye. The patient noted mild At our initial examination 6 months postoperatively, the patient irritation in the left eye 1 week postoperatively, was diagnosed complained of progressive decreased vision in his left eye since the with mild diffuse lamellar keratitis in both eyes, and was started on surgery. On examination, the uncorrected visual acuity was 20/20 prednisolone acetate, 1%, every 2 hours in both eyes. An increase in the right eye and light perception in the left eye. There was a in the interface inflammation was noted in both eyes at the 3-week brisk afferent pupillary defect present in the left eye. Biomicros- postoperative visit. Elevated intraocular pressure, measured to be copy revealed a nasally hinged flap with moderate epithelial edema 23 mmHg in both eyes, was treated with brimonidine tartrate, and microcystic edema of the epithelium peripheral to the flap in 0.2%, and timolol maleate, 0.5% (Timoptic, Merck Laboratories, the left eye. There was an optically clear fluid-filled space between West Port, PA) drops. The patient was placed on oral methylpred- the flap and the stromal bed in the left eye. Funduscopic exami- nisolone (Medrol dose pack, Pharmacia & Upjohn, Peapack, NJ), nation showed a pale optic nerve with a deeply excavated, ex- and topical prednisolone was increased to every hour in both eyes tremely thin circumferential rim and a cup-to-disc ratio of 0.99. to treat the increased interface inflammation. Best-corrected visual Corneal topography demonstrated marked central steepening in the acuity had diminished to 20/200 in the left eye at the 1-month left eye: 44.25/45.73 ϫ 002. Intraocular pressure measured using postoperative visit. The patient was started on oral prednisone, 80 applanation tonometry was less than 5 mmHg. The pressure was mg once daily, with continued hourly topical prednisolone. The 38 mmHg when measured peripherally using a Tono-Pen 2 (Au- “inflammation” persisted, and a week later the patient underwent tomated Ophthalmics, Inc., Ellicott City, MD). The patient was flap elevation and irrigation of the interface in the left eye without diagnosed with steroid-induced elevation of intraocular pressure. improvement in visual acuity. At 5 weeks postoperatively, best- Prednisolone was discontinued, oral acetazolamide, 250 mg four corrected visual acuity was 20/60 in the right eye using a Ϫ6.50 times daily, topical dorzolamide, 2% (Trusopt, Merck Laborato- rigid gas-permeable contact lens and 20/400 in the left eye. Oral ries, West Port, PA), and brimonidine, 0.25% (Alphagan, Allergan, steroids were tapered to 20 mg/day by the 6-week postoperative Irvine, CA) were added to the betaxolol. Two weeks later, the visit, topical steroids were continued hourly in both eyes, and the interface fluid had cleared in the left eye, vision remained at light patient was referred for consultation.
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