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 Table of Contents  
Year : 2019  |  Volume : 31  |  Issue : 2  |  Page : 142-144

A late-onset interface fluid syndrome post laser-assisted in situ keratomileusis: Diagnostic and therapeutic challenge

1 Department of Glaucoma, Giridhar Eye Institute, Kochi, Kerala, India
2 Department of Cornea and Refractive Surgeries, Giridhar Eye Institute, Kochi, Kerala, India
3 Department of Orbit and Oculoplasty, Giridhar Eye Institute, Kochi, Kerala, India

Date of Web Publication27-Aug-2019

Correspondence Address:
Dr. Rose Mary George
Paikada House, Vazhakulam P.O, Muvattupuzha, Ernakulam - 686 670, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/kjo.kjo_37_19

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A 43-year-old male underwent laser-assisted in situ keratomileusis and maintained good vision for 9 years. Later, he developed interface fluid syndrome secondary to steroid-induced glaucoma as a consequence of the use of steroids postoperatively for vitrectomy with silicone oil infusion for retinal detachment and cataract surgery.

Keywords: Interface fluid syndrome, pressure induced stromal keratitis, steroid-induced glaucoma

How to cite this article:
George RM, Mohan P, Nair A, Pauly M. A late-onset interface fluid syndrome post laser-assisted in situ keratomileusis: Diagnostic and therapeutic challenge. Kerala J Ophthalmol 2019;31:142-4

How to cite this URL:
George RM, Mohan P, Nair A, Pauly M. A late-onset interface fluid syndrome post laser-assisted in situ keratomileusis: Diagnostic and therapeutic challenge. Kerala J Ophthalmol [serial online] 2019 [cited 2020 Jul 11];31:142-4. Available from: http://www.kjophthal.com/text.asp?2019/31/2/142/265498

  Introduction Top

Interface fluid syndrome (IFS) or pressure-induced stromal keratitis (PISK) is a rare complication following laser-assisted in situ keratomileusis (LASIK) surgery characterized by fluid collection in the flap interface. It has been reported secondary to raised intraocular pressure (IOP), endothelial decompensation, and uveitis.[1]

  Case Report Top

A 43-year-old male, who is a known diabetic, presented with a complaint of blurring of vision in the left eye (LE) both for distance and near for 2 years. He had a history of using glasses since childhood. There was no history of contact lens wear. Barrage laser was done in the right eye (RE) for peripheral retinal degeneration in 2003. He underwent LASIK in 2008. The postoperative vision was good, and he maintained good vision in both eyes (BE) till 2017. In May 2017, he had a history of sudden drop in vision in the LE for which he consulted and was diagnosed to have retinal detachment and was advised surgery. He underwent vitrectomy with endolaser and silicone oil infusion in the LE immediately, and the postoperative vision improved but was less compared to the previous vision. After that, he was on routine follow-up and was told to have cataract in the LE which was progressing, and in February 2018, he underwent phacoemulsification with foldable intraocular lens implantation in the bag in the LE. The postoperative vision after cataract surgery did not improve; he felt deterioration in vision in the LE and presented to us for an expert opinion.

On examination, his best-corrected visual acuity in the RE was 6/12, N6, and in the LE, it was 6/24 N12; the anterior segment of the RE was normal except for the lens showing cataractous changes and IOP with Goldmann applanation tonometer (GAT) of 26 mmHg. Anterior segment of the LE showed a hazy cornea with a well-apposed flap, interface fluid, posterior-chamber intraocular lens in the bag, and the IOP with GAT was 36 mmHg. Anterior-segment optical coherence tomography (OCT) was taken which confirmed the diagnosis of interface fluid [Figure 1].
Figure 1: Anterior-segment optical coherence tomography showing clear interface in the right eye and interface fluid in the left eye

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Dilated fundus examination in the RE showed a disc with a cup-to-disc ratio (CDR) of 0.8, dense peripapillary atrophy, and tessellated background with laser marks in the superotemporal quadrant. LE fundus showed a disc with CDR of 0.8, inferior notching, dense peripapillary atrophy, tessellated background, and laser marks in the periphery [Figure 2].
Figure 2: Wide-angle fundus photography of both eyes

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The patient was diagnosed with BE steroid-induced glaucoma and LE PISK secondary to steroid-induced glaucoma. He was started on antiglaucoma medications in BE; steroid drops were tapered and stopped, and he was reassessed. On follow-up, his IOP in BE reduced to 14 and 16, but the interface fluid failed to resolve. Hence, being on maximum medical therapy for lowering IOP in the LE, he went ahead with LE trabeculectomy. Post trabeculectomy, the LE interface fluid cleared, and his vision improved to 6/12, N6.

  Discussion Top

Steroid-induced glaucoma is a late-onset postoperative complication occurring as a result of normal postoperative regimen and/or following treatments for diffuse lamellar keratitis. IFS is also known as PISK and occurs as a rare complication following LASIK surgery characterized by collection of fluid interface with a well-apposed flap above.

Clinical features: On slit lamp biomicroscopy interface fluid, minimal inflammatory cells, cystic corneal edema beyond the flap margin, and thickened flap. Corneal topography shows central corneal steepening most likely due to the interface fluid pushing the central cornea anteriorly. Intraocular pressure shows hypotony of <9 mm by applanation tonometry and hypertony on flap periphery by Tono-Pen®; Other features include worsening of visual acuity, loss of visual field and worsening symptoms with corticosteroids.[2]

Risk factors include African–American ethnicity, young age, eye related conditions like preexisting chronic open-angle glaucoma, family history of glaucoma, high myopia, previous steroid response, or any systemic diseases like history of connective tissue disease, especially rheumatoid arthritis or type 1 diabetes mellitus.[3]

Mechanisms explained in literatures regarding the etiology of the disease involve the increase of IOP causing the transudation of fluids through the endothelium from zones with high pressure to zones with low pressure. After LASIK, there is a virtual space between the flap and the stromal bed and the junction between the flap and the stroma is not able to bear the increase in pressure; therefore, the fluid gathers in the interface.[4]

In this case, diagnosis remains a challenge for the ophthalmologist due to unreliable IOP recordings; myopic disc with peripapillary atrophy makes interpretation of OCT parameters difficult, and laser marks in the fundus make perimetry interpretation also challenging.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Tourtas T, Kopsachilis N, Meiller R, Kruse FE, Cursiefen C. Pressure-induced interlamellar stromal keratitis after laser in situ keratomileusis. Cornea 2011;30:920-3.  Back to cited text no. 1
Bamashmus MA, Saleh MF. Post-LASIK interface fluid syndrome caused by steroid drops. Saudi J Ophthalmol 2013;27:125-8.  Back to cited text no. 2
Jia Z, Zhao S, Wei R, Huang Y, Zhang C, Yang R. Interface fluid syndrome: A potential lifelong complication after LASIK. A case report. Am J Ophthalmol Case Rep 2018;11:23-5.  Back to cited text no. 3
Shoji N, Ishida A, Haruki T, Matsumura K, Kasahara M, Shimizu K. Interface fluid syndrome induced by uncontrolled intraocular pressure without triggering factors after LASIK in a glaucoma patient: A case report. Medicine (Baltimore) 2015;94:e1609.  Back to cited text no. 4


  [Figure 1], [Figure 2]


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