Download Ischemic Optic Neuropathy Secondary to Severe Ocular

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

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:


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VA OS improved from count fingers (CF) to 20/70slit 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:

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VA OS 20/400
SLE: microcystic edema and “interface changes”
fundus exam: “definite RNFL whitening along the superotemporal 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
Our exam:

VA:



OD: 20/50-2 PH 20/20OS: 20/300 PH NI
CORNEA:
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
PUPILS:
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RAPD OS



by applanation tonometry:
 18 centrally
 32 temporally
by Tono-Pen:
 36 centrally
 48 temporally
A/C:

IOP OS


OD: deep, no cell/flare
OS: (hazy view) 1+ cell and
flare
LENS:


OD: clear, LASIK flap in place
OS: dense, fine SPK, stromal
edema and interface fluid
trace NSC OU
COLOR:


10/10 OD
control only OS
CASE PRESENTATION
DFE
OS: cotton-wool spots, disc
edema w/ NFL elevation, flame shaped
hemorrhage

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:

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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.
REFERENCES
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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
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Belin MW, Hannush SB, Yau CW, Schultze RL. Elevated intraocular pressure-induced interlamellar stromal keratitis.
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Galal A, Artola A, Belda J, Rodriguez-Prats J, et al. Interface corneal edema secondary to steroid-induced elevation of
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Fogla R, Rao SK, Padmanabhan P. Interface fluid after laser in situ keratomileusis. J Cataract Refract Surg
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Davidson RS, Brandt JD, Mannis MJ. Intraocular pressure-induced interlamellar keratitis after LASIK surgery. J
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