Introduction
Interface fluid syndrome (IFS) is one of the known complications after laser-assisted in situ keratomileusis (LASIK), which results from fluid collection in the LASIK flap interface.[1] Fluid accumulation in the IFS can be caused by a raised intraocular pressure (IOP),[2,3] corneal endothelial decompensation[4], and uveitis.[5] IOP measured in these eyes with Goldmann applanation tonometer (GAT) can give erroneous readings.[6–9]
The author reports a case of a bilateral interlamellar fluid and flap edema after LASIK, in a patient with undetected, advanced glaucoma, and its management.
Case Report
A 32-year-old male with an unremarkable systemic history, presented with a complaint of gradual decrease in vision in both eyes (BE). Past ocular history included LASIK in BE for high myopia, 6 years ago. He was not aware of preexisting history of ocular hypertension (OHT) or glaucoma.
On examination, the best spectacle-corrected visual acuity (BSCVA) was 6/12 in the right eye (RE) and 6/18 in the left eye (LE). Manifest refraction was –1 diopter (D) × 90° in the RE and –0.5 D/−1D × 130° in the LE. Slit-lamp examination of BE revealed an edematous, nasally hinged LASIK flap, a discoid-shaped fluid pocket at the stromal interface in anterior 1/3 stroma across the entire corneal flap, and fine pigments on the endothelium [Figure 1a-d]. The anterior chamber was deep and quiet. The pupil was mid-dilated and showed afferent pupillary defect in BE. Lens was clear and gonioscopy showed 360° open angles till the ciliary body band in BE. IOP measured by GAT over the central cornea was 18 mm Hg in RE and 20 mm Hg in LE. IOP measured by GAT in the peripheral cornea superiorly, outside the flap region was 26 mm Hg in RE and 30 mm Hg in LE. Fundus examination in BE showed an average-size optic disc, 0.9 cup–disc ratio, bipolar notch, myopic fundus, and no peripheral treatable lesion. Humphrey visual field (HVF, Carl Zeiss Meditec Inc, Dublin, CA) SITA standard 24-2 showed advanced visual field loss in BE, with no threat to the fixation on HVF 10-2. Anterior segment optical coherence tomography (AS-OCT, Optovue, Fremont, CA) showed a discoid, cleft-like hyporeflective area in the anterior stroma, corresponding to the interface fluid accumulation under the LASIK flap with a flap thickness of 243 μm in BE and an interface fluid space of 145 μm in RE and 141 μm in the LE [Figure 2a and 2b].
;)
Figure 1: (a-d) Slit-lamp photograph at presentation shows an edematous cornea in the RE (a) and LE (c). Slit section of the cornea showing interface fluid (yellow arrow) in RE (c) and LE (d). RE: Right eye, LE: Left eye
Figure 2: (a and b) Anterior segment optical coherence tomography shows a cleft-like hyporeflective area within the anterior stroma, corresponding to the interface fluid accumulation under the LASIK flap and its thickness in microns in RE (a) and LE (b). RE: Right eye, LE: Left eye
A diagnosis of high myopia post-LASIK, IFS, secondary to uncontrolled glaucoma was made. Treatment was initiated with travoprost 0.004% ophthalmic solution once daily in BE.
A week later, the cornea was clear as the flap edema had resolved and there were no signs of interface fluid. IOP measured at the central and peripheral cornea was 14 mm Hg in RE and 12 mm Hg in the LE. The patient was subsequently lost to follow-up.
Three years later, the patient presented with a complaint of decreased vision in BE. He had discontinued using topical travoprost, 3 months before the presentation. On examination, the BSCVA was hand motion in RE and counting fingers 3 m in the LE. Slit-lamp examination of BE revealed corneal edema, a disk of fluid at the flap interface. IOP measured centrally with GAT was 18 mm Hg in BE and at the peripheral cornea, outside flap was 40 mm Hg. Over the next few weeks, with topical dorzolamide hydrochloride 2% twice daily, timolol maleate 0.5% twice daily, brimonidine tartrate 0.15% thrice daily, travoprost 0.004% once daily, and tablet acetazolamide 250 mg thrice daily, IOP was reduced to 10 mm Hg in the RE and 24 mm Hg in the LE. HVF 24-2 showed advanced visual field loss in BE with a threat to the fixation, which was confirmed on HVF 10-2.
As the interface fluid persisted in the LE and IOP was 24 mm Hg on maximal medical therapy, the patient underwent trabeculectomy augmented with mitomycin C (MMC) in the LE. Postoperatively, topical prednisolone acetate 1% and moxifloxacin 0.5% four times a day were prescribed. Postoperatively, his BSCVA improved to 6/18 in the LE, the cornea was clear with no evidence of interface fluid [Figure 3a and 3b] and IOP measured with GAT was 06 mm Hg centrally and at the peripheral cornea.
Figure 3: (a-d) Slit view of the cornea a day after trabeculectomy, shows a clear cornea, resolved interface fluid with well-apposed flaps in RE (a) and LE (c). At the last follow-up visit, diffuse slit lamp examination clear cornea and good bleb in RE (b) and LE (d). RE: Right eye, LE: Left eye
On discontinuing tablet acetazolamide, IOP increased to 42 mm Hg in the RE as recorded in the peripheral cornea; hence, 2 weeks later, he underwent trabeculectomy augmented with MMC in the RE.
Postoperatively, his BSCVA improved to 6/36 in the RE. Slit-lamp examination showed a well-aligned flap with no evidence of interlamellar fluid and a clear cornea [Figure 3c and 3d]. Eight months later, at the last follow visit, the cornea was clear with no evidence of interface fluid, a diffuse, posterior bleb was noted and the IOP was 12 mm Hg in RE and 10 mm Hg in the LE, as measured by GAT at the central and peripheral cornea [Figure 3a-d]. AS-OCT confirmed the absence of interface fluid, reduction in the corneal thickness, and CCT of 557 μm in RE and 534 μm in the LE [Figure 4a and 4b]. The IOP remained in the normal range and the visual fields were stable and have not shown further progression in BE, till the last follow-up visit.
Figure 4: (a and b) Anterior segment OCT showing a reduction in the corneal thickness, no interface fluid, and well-apposed flaps in the RE (a) and LE (b). OCT: Optical coherence tomography RE: Right eye, LE: Left eye
Discussion
I report a patient who developed possibly, a bilateral steroid-induced glaucoma after LASIK, which was undetected for many years and he presented to us with cornea edema and IFS. High IOP could have increased the demand on endothelial pump function, causing flap edema, and interface fluid accumulation.[10] Flap edema in IFS is due to endothelial dysfunction, as the hydrostatic property of the flap is altered, resulting in fluid accumulation in the interface space.[11]
In this case, the challenge was to measure IOP accurately. Furthermore, the disc damage and visual field showed progression due to noncompliance with antiglaucoma medications (AGM). Trabeculectomy was required to control the IOP and arrest the glaucoma progression. Corneal edema cleared and interface fluid resolved as the IOP was initially controlled with AGM and later with trabeculectomy.
IFS may have variable clinical presentation. If the fluid accumulation under the flap is small, it may result in diffuse interface haziness and may mimic diffuse lamellar keratitis. If the fluid accumulation is pronounced, the anterior flap is separated from the posterior residual bed and it can result in a fluid pocket, which is visible clinically as a clear space in the anterior stroma. Diligent clinical examination can clinch the diagnosis and timely correct treatment can be initiated. AS-OCT is an useful modality to confirm the diagnosis and helps in the identification of the underlying pathology. In this case, at the initial visit, AS-OCT helped us to visualize the height and location of the fluid cleft and after trabeculectomy, it helped us to document the fluid resolution on the follow-up visits.
Secondary glaucoma after refractive surgery can pose certain challenges in the management. Patients with undiagnosed glaucoma can worsen after the surgery. In patients with preexisting glaucoma, LASIK poses a risk, as during the flap creation, the induced IOP rise of > 80 mm Hg, could damage an already compromised optic disc. Hence, preoperative screening for glaucoma is essential to determine which patients could be at risk, and IOP monitoring, in the postoperative period is mandatory. LASIK flap creation and excimer laser ablation alter the corneal biomechanical property and hence, IOP measurement by GAT may not be accurate.[12–14] Inaccurate IOP measurement could preclude the detection of early IOP rise. As the patients are on topical steroids after the LASIK, it is essential to monitor IOP, even in the early postoperative period, as high IOP in the steroid responder patients may result in IFS. A steroid-induced IOP increase has been reported in 5%–36% of the population, and the risk is more in young, high myopia patients.[15] Hence, the possibility of steroid-induced IOP should be kept in mind as an increase in IOP detection can be obscured by thin cornea, post-LASIK, due to an underestimation of IOP measured by GAT.[16]
IFS masks true IOP measurement using GAT, as the interface fluid acts as a compressible sponge and a IOP recording can be markedly low. Hence, if IFS is suspected, alternative means should be employed to assess true IOP. This can be achieved by IOP measurements with GAT in the peripheral cornea, outside the LASIK flap or using tonometers such as dynamic contour tonometry or TonoPen, which is relatively immune to the corneal biomechanical changes and corneal thickness.[6–9]
The importance of diagnosing IFS in a patient with preexisting glaucoma cannot be overemphasized. In our case, GAT underestimated IOP and recorded low IOP over the central cornea, but the IOP recorded in the peripheral cornea was high. After the interface fluid resolved, the IOP measurement from the central cornea was the same as in the peripheral cornea, external to the flap. This IOP reading can be considered accurate, after accounting for the thinner CCT in post-LASIK patients. Glaucomatous field loss can occur if it is not detected early, as in this case.
To conclude, clinicians must be cautious in making the selection for refractive surgery preoperatively by a thorough screening, monitoring IOP in the postoperative period, ensuring accurate IOP measurement, and meticulous slit-lamp examination for an early detection of IFS and management of OHT and glaucoma, if detected in the post-LASIK patients.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
Acknowledgment
The author would like to thank Dr. Arjun Srirampur for his help in taking slit-lamp photographs.
References
1. Lyle WA, Jin GJ. Interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after laser
in situ keratomileusis. J Cataract Refract Surg 1999;25:1009–12.
2. Hamilton DR, Manche EE, Rich LF, Maloney RK. Steroid-induced glaucoma after laser
in situ keratomileusis associated with interface fluid. Ophthalmology 2002;109:659–65.
3. Shaikh NM, Shaikh S, Singh K, Manche E. Progression to end-stage glaucoma after laser
in situ keratomileusis. J Cataract Refract Surg 2002;28:356–9.
4. Srirampur A, Kalwad A, Mansoori T, Agraharam S. Reversal of laser
in situ keratomileusis interface fluid after descemet stripping automated endothelial keratoplasty for pseudophakic bullous keratopathy. Indian J Ophthalmol 2019;67:1740–2.
5. McLeod SD, Mather R, Hwang DG, Margolis TP. Uveitis-associated flap edema and lamellar interface fluid collection after LASIK. Am J Ophthalmol 2005;139:1137–9.
6. Wheeldon CE, Hadden OB, Niederer RL, McGhee CN. Presumed late diffuse lamellar keratitis progressing to interface fluid syndrome. J Cataract Refract Surg 2008;34:322–6.
7. Park HJ, Uhm KB, Hong C. Reduction in intraocular pressure after laser
in situ keratomileusis. J Cataract Refract Surg 2001;27:303–9.
8. Fogla R, Rao SK, Padmanabhan P. Interface fluid after laser
in situ keratomileusis. J Cataract Refract Surg 2001;27:1526–8.
9. Pepose JS, Feigenbaum SK, Qazi MA, Sanderson JP, Roberts CJ. Changes in corneal biomechanics and intraocular pressure following LASIK using static, dynamic, and noncontact tonometry. Am J Ophthalmol 2007;143:39–47.
10. Macdonald JM, Geroski DH, Edelhauser HF. Effect of inflammation on the corneal endothelial pump and barrier. Curr Eye Res 1987;6:1125–32.
11. Müller LJ, Pels E, Vrensen GF. The specific architecture of the anterior stroma accounts for maintenance of corneal curvature. Br J Ophthalmol 2001;85:437–43.
12. Jarade EF, Abi Nader FC, Tabbara KF. Intraocular pressure measurement after hyperopic and myopic LASIK. J Refract Surg 2005;21:408–10.
13. Svedberg H, Chen E, Hamberg-Nyström H. Changes in corneal thickness and curvature after different excimer laser photorefractive procedures and their impact on intraocular pressure measurements. Graefes Arch Clin Exp Ophthalmol 2005;243:1218–20.
14. Chang DH, Stulting RD. Change in intraocular pressure measurements after LASIK the effect of the refractive correction and the lamellar flap. Ophthalmology 2005;112 1009.
15. Dawson DG, Schmack I, Holley GP, Waring GO 3rd, Grossniklaus HE, Edelhauser HF. Interface fluid syndrome in human eye bank corneas after LASIK:Causes and pathogenesis. Ophthalmology 2007;114:1848–59.
16. Emara B, Probst LE, Tingey DP, Kennedy DW, Willms LJ, Machat J. Correlation of intraocular pressure and central corneal thickness in normal myopic eyes and after laser
in situ keratomileusis. J Cataract Refract Surg 1998;24:1320–5.
