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 OphthalmologyDanville, PA

* No financial interest

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.

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

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

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.

CASE PRESENTATION

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

Our exam:

CASE PRESENTATIONDFE OS: cotton-wool spots, disc DFE OS: cotton-wool spots, disc edema w/ NFL elevation, flame shaped edema w/ NFL elevation, flame shaped hemorrhagehemorrhage

HVF 30-2 OS (2 weeks later): Superior altitudinal defect

CASE PRESENTATION

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.

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

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

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.

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