Diagnosis of post-LASIK occult Chandler syndrome

Abstract

Mocan et al.1 have described a patient who was diagnosed with Chandler syndrome, one of the entities comprising the iridocorneal endothelial (ICE) syndrome, after unilateral iris distortion and glaucoma following bilateral laser in situ keratomileusis (LASIK). We have treated a similar patient, a 36-year-old woman with a refractive error of −2.00 +1.50 × 180 in the right eye and −2.50 + 1.75 × 165 in the left eye who had uneventful bilateral LASIK procedures. Preoperative testing revealed no significant abnormalities; the intraocular pressure (IOP) by applanation was 17 mm Hg bilaterally and the central pachymetry by ultrasound was 509 μm in the right eye and 514 μm in the left eye. One day postoperatively, the uncorrected visual acuity (UCVA) was 20/20 in both eyes, but on the third postoperative day, the patient awoke with blurry vision in the right eye. When she was seen 4 days postoperatively, the UCVA in the right eye had dropped to 20/30 and diffuse inflammation was noted in the interface. Hourly prednisolone acetate 1% eyedrops were started to treat presumed diffuse lamellar keratitis. After 1 day of this intensive topical corticosteroid therapy, the interface inflammation did not improve so the flap was lifted and the interface was cultured and irrigated. Over the ensuing week, the UCVA improved to 20/20 and the corneal inflammation subsided. At this time, cornea guttata were first noticed on the right endothelial surface. Interface fluid syndrome was considered a possibility, but no interface fluid was noted on careful inspection and at no time was elevated IOP noted centrally or peripherally. Over the course of the next year, the patient was seen on numerous occasions, complaining of intermittent episodes of blurry vision in the right eye, with a drop in UCVA to 20/25 to 20/30 with normal IOP. One year post-LASIK, the UCVA dropped to 20/40; the IOP was 19 mm Hg and the central pachymetry, 526 μm. Transient endothelial dysfunction related to anterior segment inflammation, as described following LASIK by McLeod et al.,2 or as an early manifestation of Fuchs corneal dystrophy was diagnosed. Bimatoprost, brimonidine, and timolol eyedrops, in sequence, were added to the treatment regimen; initially, the UCVA improved in proportion to a decrease in central corneal thickness. However, the IOP became impossible to control, ranging between 29 mm Hg and 35 mm Hg, and the patient was referred to a glaucoma specialist. The consultant noted a “beaten metal” appearance of the endothelium and a diagnosis of possible occult Chandler syndrome was suggested. Subsequently, specular and confocal microscopy revealed endothelial changes consistent with Chandler syndrome. Three years after the LASIK procedure, the patient developed corneal decompensation with persistent stromal and epithelial microcystic edema in the right eye. Penetrating keratoplasty was performed, and immunohistochemical studies of the resected cornea demonstrated staining of the endothelial cells for cytokeratins, consistent with the ICE syndrome. The IOP continued to fluctuate and eventually remained elevated, ranging from 26 mm Hg to 45 mm Hg; this led to episodic corneal graft edema. Glaucoma tube shunt surgery with insertion of an Ahmed valve was performed. Following this procedure, the IOP has remained under control, the cornea and lens have remained clear, and no pathological optic disc cupping or visual field changes have developed. At the time of the patient's most recent examination, 1 year after Ahmed valve placement and 2 years after PKP, the UCVA in the right eye was 20/30 (best corrected acuity 20/20) and the IOP was 18 mm Hg. Our patient and the one reported by Mocan et al.1 demonstrate the importance of considering the possibility of an occult ICE syndrome in a post-LASIK patient presenting with elevated IOP, corneal edema, and/or iris abnormalities, especially when these findings are unilateral. The onset of ICE syndrome symptoms in both patients may have been unrelated to the LASIK surgery. Mocan et al. suggest that in vivo confocal microscopy should be performed in all patients before refractive corneal procedures. The limited availability of confocal microscopy at present, combined with the relatively low incidence of the ICE syndrome, makes this impractical for most ophthalmologists. It is unclear whether the LASIK procedure aggravates or accelerates the progression of the ICE syndrome, as would be suggested by these 2 cases. Aggressive management of the corneal condition and the IOP can result in a favorable outcome, assuming these interventions are performed in a timely manner.