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Rachel E. Peck, MD * Kendall R. Dobbins, MD *

Ischemic Optic Neuropathy Secondary to Severe Ocular Hypertension Masked by Interface Fluid in a Post-LASIK Eye. Rachel E. Peck, MD * Kendall R. Dobbins, MD *. Geisinger Medical Center, Department of Ophthalmology Danville, PA. * No financial interest. PURPOSE.

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Rachel E. Peck, MD * Kendall R. Dobbins, MD *

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  1. Ischemic Optic Neuropathy Secondary to Severe Ocular Hypertension Masked by Interface Fluid in a Post-LASIK Eye Rachel E. Peck, MD* Kendall R. Dobbins, MD* Geisinger Medical Center, Department of Ophthalmology Danville, PA * No financial interest

  2. PURPOSE • To present a case of ischemic optic neuropathy arising from elevated intraocular pressure (IOP), due to hyphema, that was masked by interface fluid in a post-LASIK eye.

  3. CASE PRESENTATION • 51 year old male with bilateral decreased vision and eye pain • States a large piece of wood flew off cutting table and struck him on the nose and brow • Exam revealed bilateral hyphemas • POH: LASIK OU in 2001 • Treated by outside ophthalmologist for 10 days prior to being seen at our clinic • Right eye (OD) had a mild hyphema that cleared by day 3 • Left eye (OS) had a more complicated course, which prompted referral to our center

  4. CASE PRESENTATION • Summary of Referring Physician’s Exam of OS • In the first 3 days after the injury: • VA OS improved from count fingers (CF) to 20/70- • slit lamp exam (SLE): microcystic edema and “interface changes” • fundus exam: (poor view) 0.15 c/d, normal macula, and “peripheral retinal hemorrhage versus vitreous hemorrhage” • Day 5: • VA OS decreased to 20/400 ph 20/200 • fundus exam: (poor view) “subtle thickening of the retinal nerve fiber layer (RNFL)” along the supero-temporal arcade

  5. CASE PRESENTATION • Summary of Referring Physician’s Exam of OS • Day 10: • VA OS 20/400 • SLE: microcystic edema and “interface changes” • fundus exam: “definite RNFL whitening along the supero-temporal arcade and at 6 o'clock off the optic nerve” • Medications: prednisolone QID, homatropine BID, dorzolamide BID • IOP by applanation tonometry was never reported to be higher that 25 OS (day 5) • 10 days after the initial injury, the patient was referred to our center for evaluation.

  6. VA: OD: 20/50-2 PH 20/20- OS: 20/300 PH NI PUPILS: RAPD OS IOP OS by applanation tonometry: 18 centrally 32 temporally by Tono-Pen: 36 centrally 48 temporally CORNEA: OD: clear, LASIK flap in place OS: dense, fine SPK, stromal edema and interface fluid A/C: OD: deep, no cell/flare OS: (hazy view) 1+ cell and flare LENS: trace NSC OU COLOR: 10/10 OD control only OS CASE PRESENTATION Our exam:

  7. HVF 30-2 OS (2 weeks later): Superior altitudinal defect CASE PRESENTATION • DFE OS: cotton-wool spots, disc edema w/ NFL elevation, flame shaped hemorrhage

  8. Based on our exam findings, we felt that the patient had developed an ischemic optic neuropathy from unrecognized acute IOP elevation persisting over several days. The patient was started on aggressive pressure reducing medications. IOP was measured in centrally and peripherally using both applanation and Tono-Pen all follow-up visits. As the IOP improved, the interface fluid decreased. Best-corrected visual acuity (BCVA) OS did not exceed 20/150. CASE PRESENTATION

  9. INTERFACE FLUID SYNDROME • Uncommon, post- LASIK complication that typically occurs in steroid responders and presents clinically as corneal edema that closely resembles Diffuse Lamellar Keratitis (DLK) • First described in 19991 • Proposed names include: “pseudo-DLK,” interface fluid syndrome, pressure induced interface keratitis, pressure induced interlamellar stromal keratitis (PISK), interlamellar stromal keratopathy induced by elevated IOP • In a review of the literature, nearly all cases of interface fluid syndrome have been due to a steroid response to topical drops and were typically exacerbated or prolonged with more aggressive steroid regimes in order to treat mistakenly diagnosed DLK1-11

  10. INTERFACE FLUID SYNDROME • Interface fluid in a post-LASIK eye can manifest clinically as decreased VA, myopic shift in refraction, stromal edema or interface fluid on slit lamp exam (SLE), increase in pachymetry measurements, steepening of corneal topography, or inappropriately low IOP measurements2 • Pathophysiology: • High intraocular pressure diffusion of aqueous humor across the corneal endothelium into the stromal interface created by the flap pocket of fluid accumulates at the lamellar interface3,12 • IOP measurement inaccuracies arise because applanation tonometry reflects the pressure of the interface fluid pocket and not the true intraocular pressure12

  11. CONCLUSION • Our patient developed ocular hypertension as a result of a hyphema. After several days of suspected acute IOP elevation (which was masked by interface fluid), ischemic optic neuropathy developed. • Although interface fluid accumulation and inaccurate IOP measurements after LASIK have been reported, this case is the first to associate interface fluid syndrome with subsequent acute ischemic optic neuropathy after trauma (hyphema). • Six years is the longest post-LASIK interval in which accumulation of interface fluid has been reported.

  12. REFERENCES • Lyle WA, Jin GLC. Interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after in situ keratomileusis. J Cataract Refract Surg 1999;25:1009-12. • Dawson DG, Hardten DR, Albert DM. Pocket of fluid in the lamellar interface after penetrating keratoplasty and laser in situ keratomileusis. Arch Ophthalmol 2003;121:894-96. • Hamilton DR, Manche EE, Rich LF, Maloney RK. Steroid-induced glaucoma after laser in situ keratomalieusis associated with interface fluid. Ophthalmology 2002;109(4):659-65. • Belin MW, Hannush SB, Yau CW, Schultze RL. Elevated intraocular pressure-induced interlamellar stromal keratitis. Ophthalmology 2002;109(10):1929-33. • Nordlund ML, Grimm S, Lane S, Holland EJ. Pressure-induced interface keratitis: a late complication following LASIK. Cornea 2004;23(3): 225-34. • Galal A, Artola A, Belda J, Rodriguez-Prats J, et al. Interface corneal edema secondary to steroid-induced elevation of intraocular pressure simulating diffuse lamellar keratitis. J Refract Surg 2006;22(5):441-7. • Fogla R, Rao SK, Padmanabhan P. Interface fluid after laser in situ keratomileusis. J Cataract Refract Surg 2001;27(9):1526-8. • Shaikh NM, Shaikh S, Singh K, Manche E. Progression to end-stage glaucoma after laser in situ keratomileusis. J Cataract Refract Surg 2002;28(2):356-9. • Davidson RS, Brandt JD, Mannis MJ. Intraocular pressure-induced interlamellar keratitis after LASIK surgery. J Glaucoma 2003;12(1):23-6. • Rehany U, Bersudsky V, Rumult S. Paradoxical hypotony after laser in situ keratomileusis. J Cataract Refract Surg 2000;26:1823-26. • Portellinha W, Kuchenbuk M, Nakano K, Oliveira M. Interface fluid and diffuse corneal edema after laser in situ keratomileusis. J Refract Surg 2001;17:S192-95. • Samuelson TW. Refractive surgery in glaucoma. Curr Opin Ophthalmol 2004;15:112-18.

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