Interface fluid after LASIK: misleading tonometry can lead to end-stage glaucoma

Abstract

We are interested in the recent case report on interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after laser in situ keratomileusis by Lyle and Jin.1 We recently evaluated a similar case: A 58-year-old man was referred to us for consultation following bilateral laser in situ keratomileusis (LASIK). The preoperative cycloplegic refraction was −10.00 −0.25 × 110 in the right eye and −8.25 −1.50 × 140 in the left, and the best corrected visual acuity was 20/20 in each eye. The referring doctor reported that 3 weeks after surgery, the left eye developed what appeared to be a diffuse lamellar keratitis, characterized by diffuse granular haze and microcystic epithelial edema. The eye was treated aggressively with topical prednisolone acetate 1% and topical sodium chloride 5%. The edema apparently improved, but the flap became hazy and the vision was poor. Applanation tonometry was reported to be normal, but since significant cupping was noted in the left optic nerve, topical betaxolol was added to the treatment and the prednisolone acetate tapered. When we examined the patient for the first time 6 months postoperatively, he complained about poor vision in the left eye since LASIK and stated that the vision had been getting progressively worse. He was using prednisolone acetate 1% drops twice a day, sodium chloride 5% 4 times a day, and betaxolol twice a day. The uncorrected visual acuity was 20/20 in the right eye and light perception in the left. The left eye showed a brisk afferent pupillary defect. Biomicroscopy of the left eye revealed a nasal hinged flap with moderate epithelial edema and epithelial edema outside the flap border superiorly. There was a fluid-filled gap in the interface between the flap and the stromal bed. The anterior chamber was deep and quiet, and the lens was clear. The optic nerve was pale with a cup-to-disc ratio of 1.0. Intraocular pressure (IOP) was less than 3 mm Hg in the left eye by Goldmann applanation tonometry but 38 mm Hg by Tono-Pen 2 (Mentor Ophthalmics). Steroid-induced glaucoma was diagnosed in the left eye. Prednisolone was discontinued, and dorzolamide and brimonidine were added to the betaxolol the patient was using. The patient was referred for glaucoma specialist care. The case described by Lyle and Jin and our patient share some features. Both presented a layer of fluid in the interface; both appeared to have had uneventful LASIK followed by diffuse lamellar keratitis; and both presented steroid-induced IOP elevation and a falsely low IOP reading by Goldmann tonometry. Nevertheless, in our case the patient did not have epithelial ingrowth. We agree with Lyle and Jin's observation that falsely low IOP measurements resulted from the easy compressibility of the fluid-filled space between the back of the corneal flap and the stromal bed. However, we disagree that the source of the fluid is epithelial ingrowth. Rather, we believe the fluid is a transudate from the elevated IOP. In our experience, eyes with epithelial ingrowth after LASIK never develop an interface fluid-filled space in the absence of elevated IOP. Regardless of the source of the interface fluid, we agree that clinicians should be aware that the presence of this fluid may lead to erroneously low IOP measurements and that situation, if unrecognized, can lead to severe glaucomatous damage. Jacobo Najman-Vainer MD Ronald J. Smith MD Robert K. Maloney MD, MA (OXON) Los Angeles, California, USA