Am J Ophthalmol. 2005 Jun;139(6):1137-9.


Uveitis-associated flap edema and lamellar interface fluid collection after LASIK.

McLeod SD, Mather R, Hwang DG, Margolis TP.

Francis I. Proctor Foundation and the Department of Ophthalmology, University of California-San Francisco, 10 Kirkham Street, San Francisco, CA 94143, USA. smcleod@itsa.ucsf.edu

PURPOSE: To report two cases of corneal pathology associated with anterior uveitis after laser in situ keratomileusis (LASIK).

DESIGN: Observational case report.

METHODS: A 47-year-old man and a 50-year-old woman who experienced vision loss and corneal changes associated with acute anterior uveitis after LASIK were examined.

RESULTS: The 47-year-old man, who had undergone LASIK for low myopia developed an interlamellar fluid pocket at the level of the flap interface, whereas the 50-year-old woman, who underwent LASIK for hyperopia, developed marked flap edema without interface fluid collection.

CONCLUSIONS: These two cases demonstrated acute corneal fluid accumulation associated with episodes of acute anterior uveitis in eyes that had undergone LASIK. Uveitis should be considered a risk factor for vision threatening corneal complications after LASIK.

J Cataract Refract Surg. 2005 May;31(5):922-9.


Noninflammatory flap edema after laser in situ keratomileusis associated with asymmetrical preoperative corneal pachymetry.

Loh RS, Hardten DR.

Minnesota Eye Consultants, Minneapolis, Minnesota, USA.

PURPOSE: To report persistent unilateral flap edema following laser in situ keratomileusis (LASIK) in patients with asymmetrical central corneal thickness.

SETTING: Minnesota Eye Consultants, Minneapolis, Minnesota.

METHODS: Retrospective, noncomparative interventional case series.

RESULTS: We examined 6 eyes of 3 patients with asymmetrical preoperative pachymetry who developed persistent unilateral flap edema after uneventful myopic LASIK in the eye with thicker preoperative pachymetry. All cases had asymmetrical preoperative pachymetry with flap edema developing in the eye with higher preoperative mean central corneal thickness (CCT) values, preoperative mean CCT subject eye 622 microm (range 556-664 microm) versus fellow eye 583 microm (range 510-621 microm). There was no associated ocular inflammation or rise in intraocular pressure. Significant flap edema resolved on a combination treatment of topical steroid and hypertonic saline.

CONCLUSIONS: Laser in situ keratomileusis can cause temporary endothelial cell dysfunction or stress, which manifests as temporary flap edema and subclinical corneal thickening. The edema appears to be limited to the actual flap and there was no loss of epithelial integrity in these eyes and no clinically noticeable interface fluid. This new clinical entity appears to occur in patients with asymmetrical preoperative corneal pachymetry and is associated with postoperative specular microscopy abnormalities. In cases with unexplained asymmetrical corneal thickness, preoperative evaluation should include specular microscopy to evaluate for risk features that may increase the chances of a slower postoperative recovery.

Ophthalmology. 2002 Apr;109(4):659-65.

Steroid-induced glaucoma after laser in situ keratomileusis associated with interface fluid.

Hamilton DR, Manche EE, Rich LF, Maloney RK.

Jules Stein Eye Institute, University of California-Los Angeles, Los Angeles, CA 90095, USA.

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.

Interface Corneal Edema Secondary to Steroid-induced Elevation of Intraocular Pressure Simulating Diffuse Lamellar Keratitis

Journal of Refractive Surgery Vol. 22 No. 5 May 2006

Ahmed Galal, MD, PhD; Alberto Artola, MD, PhD; Jose Belda, MD, PhD; Jose Rodriguez-Prats, MD, PhD; Pascual Claramonte, MD, PhD; Antonio Sánchez, MD, PhD; Oscar Ruiz-Moreno, MD, PhD; Jesús Merayo, MD, PhD; Jorge Alió, MD, PhD

PURPOSE

To describe interface corneal edema secondary to steroid-induced elevation of intraocular pressure (IOP) following LASIK.

METHODS
Retrospective observational case series. Diffuse interface edema secondary to steroid-induced elevation of IOP was observed after LASIK simulating diffuse lamellar keratitis (DLK) in 13 eyes. Mean patient age was 31.4±5.3 years. Patients were divided into two groups according to provisional misdiagnosis: DLK group (group 1) comprised 11 eyes and infection group (group 2) comprised 2 eyes (microbial keratitis). Mean follow-up was 8.1±0.5 weeks.

RESULTS
In the DLK group, typical diffuse haze was confined to the interface and extended to the visual axis, impairing vision in all eyes. Provisional diagnosis was late-onset DLK and topical steroids were started. Repeat examination showed elevated IOP as measured at the corneal center and periphery using applanation tonometry (mean 19.1 mmHg and 39.5 mmHg, respectively), causing interface edema with evident interface fluid pockets. Steroids were stopped and topical anti-glaucoma therapy was started. The interface edema decreased and at the end of follow-up the corneal transparency was restored and IOP dropped to normal values. The infection group demonstrated a microbial keratitis-like reaction and underwent flap lifting and interface wound debridement and biopsy with administration of fortified antibiotics and steroids. After elevated IOP was detected, steroids and antibiotics were stopped and topical anti-glaucoma therapy was started, resulting in the resolution of the interface edema.

CONCLUSIONS
Interface fluid syndrome secondary to steroid-induced elevation of IOP might develop in steroid responders after LASIK with a misleading clinical picture simulating DLK or infectious keratitis. Management includes stopping topical steroids and starting topical anti-glaucoma therapy. [J Refract Surg. 2006;22:441-447.]

Ophthalmic Surg Lasers Imaging. 2008 Jul-Aug;39(4 Suppl):S80-2.

High-resolution imaging of complicated LASIK flap interface fluid syndrome.

Ramos JL, Zhou S, Yo C, Tang M, Huang D.
Doheny Eye Institute, Los Angeles, California, USA.

The authors report a case of post-LASIK interface fluid syndrome that led to epithelial ingrowth, a sequelae that had not been reported to date. The interface fluid was caused by steroid-induced ocular hypertension. On post-LASIK day 49, the interface fluid, epithelial ingrowth, and noncellular reflective deposits were visualized by confocal microscopy and high-resolution Fourier-domain optical coherence tomography. No inflammatory cells or infectious organisms were seen. These high-resolution imaging technologies were useful in the noninvasive evaluation of the location and nature of flap interface pathologies at the microstructural level.

Not a peer-reviewed article:

Ophthalmology Management
Sept. 09

http://www.ophmanagement.com/article.as ... cle=103389

Steven Safran, MD prefers PRK over LASIK for the following reasons:

► It is more sparing of corneal tissue and nerves, thus posing less risk of postop ectasia or dry eye.
► The absence of a flap eliminates the risks of striae/microstriae, fine flap irregularities, epithelial ingrowth, flap dislocation and diffuse lamellar keratitis.
► Studies on cadaver eyes with a history of LASIK while alive showed fluid in the interface on all eyes. One concern is fluid collecting there if cataract, retina or glaucoma surgery is needed (or if inflammation, uveitis, other diseases affect the eye), as fluid tends to collect in potential spaces when there is inflammation or edema.
► PRK is less frightening to the patient during surgery (no suction ring, no mechanical contraptions etc.)
► Results are easier to enhance — just do PRK again. “Some of us hate re-lifting flaps because of increased epithelial in-growth risk,” Dr. Safran noted.
► The quality of vision in the long run is better with PRK in Dr. Safrans experience.