To the Editor:
Interface fluid syndrome (IFS) is a flap-related complication of LASIK surgery, first reported in the literature by Lyle and Jin in 1999.1 Symptoms usually appear 1 week to 2 months after uncomplicated LASIK. Clinically, it is associated with diffuse, nongranular haze or a distinct fluid-filled cleft in the LASIK interface wound confined to the central and paracentral areas usually caused by steroid-inducing ocular hypertension.1,2 Differential diagnosis with diffuse lamellar keratitis is warranted.
Interface fluid syndrome has also been reported to be caused by uveitis,3 vitreoretinal surgery,4 or decreased endothelial cell density. It results in transudation of aqueous humor across the corneal endothelium and stromal lamellae of the residual stromal bed with subsequent fluid accumulation and swelling in the hypo-cellular primitive LASIK wound.5
Interface fluid syndrome after cataract surgery without associated endothelial cell dysfunction has not been reported previously.
A 47-year-old man underwent bilateral LASIK for low myopia without complications. Uncorrected distance visual acuity (UDVA) 1 year after surgery was 20/20 in both eyes.
Three years after surgery, the patient presented with glare and bad adaptation to darkness. On examination, posterior subcapsular cataracts +3 were noted in the right eye.
Phacoemulsification with in-the-bag intraocular lens (IOL) implantation (18.50 D, double-K SRK/T) was performed in the right eye. One day after surgery, he reported blurred vision, pain, and photophobia. Clinically, he presented with paracentral nongranular haze in the interface wound concordant with stage II IFS (Fig).5 Central applanation intraocular pressure (IOP) was 18 mmHg, but peripheral to the LASIK flap, IOP was 38 mmHg. Viscoelastic material retained in the eye was the presumed etiology of the high IOP. After anterior chamber drainage (expression of the posterior lip of the cataract wound), IOP decreased to 16 mmHg, and topical hypotensive drugs were instilled the following day. Two days later, anterior chamber drainage of IFS was resolved (see Fig), with a final UDVA of 20/20 in the right eye.
Figure. A) Corneal optical coherence tomography (OCT) showing fluid accumulation in the flap–stroma interface with optical pachymetry of 602 μm. The arrow indicates the interface wound. B) Slit-lamp examination shows corneal edema with paracentral nongranular haze concordant with stage II interface fluid syndrome. C) Corneal OCT shows resolution of the condition with optical pachymetry of 494 μm. D) Slit-lamp examination shows resolution of the corneal edema and haze.
This case documenting interface fluid collection and flap edema represents the first reported case of IFS after raised IOP following cataract surgery.
Viscoelastic material such as hyaluronate retained in the eye after cataract surgery is frequently responsible for postoperative IOP elevation.
Any condition that increases IOP is a potential cause of IFS. Interface fluid syndrome may even appear years after LASIK surgery. Interface fluid syndrome most commonly presents 1 week to a few months after surgery in steroid responsive patients. In this case, IFS occurred 3 years after LASIK. There are some reports of IFS occurring 4 years after LASIK.
To avoid missing intraocular hypertension that could lead to permanent glaucoma-related damage, it is essential to obtain accurate IOP readings peripheral to the LASIK flap.3
Previous histopathologic and ultrastructural studies on human corneas with LASIK surgery have shown that LASIK interface wounds heal in a limited and incomplete fashion,5 making these wounds susceptible to flap-related complications such as IFS years after LASIK.
Ophthalmologists should be aware that any condition that increases IOP or damages endothelial cell function years after LASIK may precipitate IFS. Strict removal of viscoelastic material is warranted.
Ester Carreño, MD
Alejandro Portero, MD
David J. Galarreta, MD, PhD
Jesús M. Merayo, MD, PhD
- Lyle WA, Jin GJ. Interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after laser in situ keratomileusis. J Cataract Refract Surg. 1999;25(7):1009–1012. doi:10.1016/S0886-3350(99)00083-8 [CrossRef]
- Hamilton DR, Manche EE, Rich LF, Maloney RK. Steroid-induced glaucoma after laser in situ keratomileusis associated with interface fluid. Ophthalmology. 2002;109(4):659–665. doi:10.1016/S0161-6420(01)01023-5 [CrossRef]
- McLeod SD, Mather R, Hwang DG, Margolis TP. Uveitis-associated flap edema and lamellar interface fluid collection after LASIK. Am J Ophthalmol. 2005;139(6):1137–1139. doi:10.1016/j.ajo.2004.12.018 [CrossRef]
- Senthil S, Rathi V, Garudadri C. Misleading Goldmann applanation tonometry in a post-LASIK eye with interface fluid syndrome. Indian J Ophthalmol. 2010;58(4):333–335. doi:10.4103/0301-4738.64133 [CrossRef]
- Dawson DG, Schmack I, Holley GP, Waring GO III, Grossniklaus HE, Edelhauser HF. Interface fluid syndrome in human eye bank corneas after LASIK: causes and pathogenesis. Ophthalmology. 2007;114(10):1848–1859. doi:10.1016/j.ophtha.2007.01.029 [CrossRef]