Delayed-onset pressure-induced interlamellar stromal keratitis (PISK) and interface epithelial ingrowth 10 years after laser-assisted in situ keratomileusis

Abstract

Purpose

To report a case of pressure-induced interlamellar stromal keratitis (PISK) 10 years after laser assisted in situ keratomileusis (LASIK).

Observations

A case of a 36-year-old man who underwent LASIK and presented with PISK 10 years later. Before presenting to our department he consulted elsewhere for red eye, decreased visual acuity, foreign body sensation, and pain on the RE for 1 week. He was then prescribed topical prednisolone six times per day and was lost to follow-up. On examination and after 1 month of continuous use of steroids uncorrected distance visual acuity (UCDV) was 20/400 in the right eye (RE) and 20/20 in the left eye (LE). Best corrected visual acuity was 20/80 on the RE. The Goldmann intraocular pressure (IOP) was 26 and 17 mmHg in the RE and LE, respectively. Slit lamp biomicroscopy revealed fluid in the interface and epithelial ingrowth. Fundoscopic examination results were normal in both eyes. Treatment was initiated with topical brimonidine tartrate 0.2%, timolol 0.5%, and dorzolamide 2.0% BID. Once the pressure was controlled the patient was scheduled for mechanical debridement of the epithelial ingrowth with significant improvement of UCVA (20/25).

Conclusions

Refractive surgeons should be aware of PISK as a potential complication of LASIK even years after the procedure. Intraocular pressure can be misleading, and diligent and careful examination are key to diagnosis and treatment of this potentially blinding complication.

1. Introduction

Laser in situ keratomileusis (LASIK) is the most scrutinized and studied laser vision correction procedure.¹ Interface epithelial ingrowth is a rare complication and can impair vision significantly. Although most reported cases are mild and visually insignificant, mechanical removal may be necessary in some cases.² Another rare complication of LASIK¹ is interface fluid syndrome (IFS), also known as pressure-induced interlamellar stromal keratitis (PISK), characterized by fluid collection at the flap interface due to elevated intraocular pressure, which was described by Belin et al. as a type of interface haze and edema that occurs several weeks to months after LASIK.³ We describe a case of PISK and epithelial ingrowth 10 years after refractive surgery.

2. Case report

A 36-year-old male patient presented to the Department of Cornea and Refractive Surgery at the Instituto de Oftalmologia Fundacion Conde de de Valenciana IAP, in Mexico City, reporting blurred vision in his right eye for 2 years. He had undergone LASIK in both eyes (OU) 10 years ago with no other relevant medical history. He was examined 1 month prior to his visit and was treated with topical prednisolone 1% drops every 3 hours.

Upon clinical examination, uncorrected distance visual acuity (UCDV) was 20/400 in the right eye (RE), which improved to 20/80 with a pinhole, and 20/20 in the left eye (LE). The Goldmann intraocular pressure (IOP) was 26 and 17 mmHg in the RE and LE, respectively. RE refraction was +3.00 = −2.00 × 30. Slit lamp biomicroscopy revealed a large temporal patch of intraepithelial growth reaching the visual axis, fluid accumulation between the flap and stromal bed, sub-epithelial edema, and microbullae (Fig. 1A), on the LE no remarkable findings were noted. The LASIK flap was intact with a superior hinge in both eyes. Fundoscopic examination results were normal in both eyes. Oculus Pentacam curvature sagittal map demonstrating irregular astigmatism in the same area as the intraepithelial ingrowth (Fig. 1A). Pachymetry map (Fig. 2B) and optical coherence tomography (OCT) revealed a central corneal thickness of 579 μm interface opacities and fluid collection in the interface (Fig. 2C). Prednisolone was stopped and combined Brimonidine Tartrate 0.2%, Timolol 0.5% and Dorzolamide 2.0% BID was started (Krytantek, Laboratorios Sophia, Mexico).

Fig. 1.

A) Curvature sagittal map showing irregular astigmatism in the same area as the intraepithelial ingrowth.

B) Corneal thickness map reporting a central pachymetry of 579 μm. C) Optical coherence tomography of the Right Eye showing the fluid accumulated between the flap and the stromal bed.

Fig. 2.

A) General illumination slit-lamp image showing intraepithelial growth around pupil margin (arrow).

B) Diffuse illumination showing epithelial ingrowth and irregular flap border (arrow). C) Anterior segment OCT showing interface fluid (green arrows) and intraepithelial ingrowth (yellow arrow). D) 1 week after procedure showing general illumination without epithelial ingrowth. E) Diffuse illumination 1 week after procedure with residual edema (arrow) and without epithelial ingrowth. F) 1 week after procedure AS-OCT without fluid or epithelial ingrowth. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

After 36 h of treatment, the patient reported improvement in vision and a decrease in symptoms. On examination, an uncorrected visual acuity of 20/200 improved to 20/40 with refraction and IOP of 14 mmHg with no visible interface fluid detectable on clinical examination. Pressure-lowering medications were continued for 1 month and eventually tapered and discontinued after 3 months. However, because of glare and irregular astigmatism, the patient was scheduled for interface debridement 6 months after initial presentation. (Fig. 1 B, C); Briefly, topical 0.5% tetracaine was administered immediately prior to the procedure. A sterile drape and wire lid speculum was placed on the right eye. The flap was lifted using a LASIK spatula. Epithelial ingrowth was scraped from the posterior surface of the flap and stromal bed using a blunt photorefractive keratectomy spatula. Both stromal faces (both stromal and flap surfaces) were exposed to a microsponge with 50% alcohol and then 0.02% mitomycin for 40 seconds. After repositioning the flap, the interface was irrigated with a balanced saline solution followed by 0.5% moxifloxacin, and a bandage contact lens was placed. The patient was treated postoperatively with 0.5% moxifloxacin and 1% prednisolone acetate QID. Once the epithelium healed, the bandage contact lens was removed. On the first day after the intervention, the UCVA in the RE was 20/30 and 1 week after the surgery it was 20/20 (Fig. 1 D, E, F). Topical steroids were tapered over a 2-week period.

3. Discussion

PISK after LASIK is a rare but visually threatening postoperative complication. Diffuse lamellar keratitis (DLK) also known as “Sands of Sahara Syndrome” and pressure-induced interlamellar stromal keratitis (PISK)³ are both LASIK complications with potential overlapping clinical manifestations4, 5, 6 and has to be considered as differential diagnosis, due to the clinical aggravation that can follow the use of steroids in PISK.⁴ DLK is an idiopathic interface inflammation that typically occurs within the first postoperative week, with clinical features that range from asymptomatic infiltration confined to the interface to stromal necrosis.^4,5 Inflammatory mononuclear cells and granulocytes, typically seen in patients with DLK, are absent in patients with PISK⁶ [6]. We suspect DLK was the initial diagnosis done elsewhere and thus intensive topical steroids were prescribed.

PISK is a disorder with a DLK-like interface haze caused by steroid-induced ocular hypertension after LASIK⁶ and the presence of fluid at the interface between the flap and the stromal bed. Kurian et al. demonstrated the findings of confocal microscopy in a patient with interface haze and elevated IOP after LASIK who had microlacunae, which was thought to be a consequence of stromal edema.⁷ The clinical findings are not associated with an accumulation of inflammatory cells but are caused by edema.

PISK is diagnosed by careful examination, with observation of the interface where fluid may accumulate. It may be essential in follow-up examinations to assess resolution of fluid collection using anterior segment OCT⁸ or high-resolution Scheimpflug imaging.⁹ Intraocular pressure may be misleading^10,11 as PISK may masquerade with falsely low IOP readings. Many refractive surgeons do not measure IOP on the first day after corneal refractive surgery because of concerns about causing further insult to the corneal epithelium. However, IOP should be measured during subsequent postoperative visits. Therefore, in the presence of low IOP and interface fluid syndrome IOP lowering medications should be considered. Some authors recommend performing an OCT scan if SMILE or LASIK is performed if a patient presents with an unexplainable vision loss or if there is an increase in IOP compared with the previous visit.¹² Kim et al. underscore the significance of intraocular pressure (IOP) management in post-refractive surgery eyes, particularly after LASIK, as a means to mitigate potential complications.¹³

The treatment of PISK involves cessation of steroids and initiation of IOP-lowering medications. Beta-blockers are the first-choice medications and, in case of IOP-lowering insufficient response, perhaps IV mannitol or oral diuretics. Unlu et al. emphasized that there have been several publications detailing PISK regarding the use of antiglaucoma medications and discontinuation of topical steroids in its management.¹⁴ Untreated elevated IOP can lead to optic nerve damage, and it is essential to differentiate DLK from PISK because the latter worsens with steroids, which is the typical treatment for DLK.¹⁵

Epithelial ingrowth after LASIK has been reported to occur in 0–20% of cases, with a cumulative mean of 4.3% in a review of LASIK publications.^5,16,17 Most cases are self-limited, occurring at the edge of the flap and extending inward less than 0.5 mm, without clinical relevance. Surgical removal is required when epithelial ingrowth approaches the edge of the pupil and decreases vision or induces nighttime glare. However, for symptomatic patients, treatment options may include laser ablation or surgical lifting of the flap and scraping of the cells. This case report involved mechanical removal with complete resolution of the symptoms.

Patients with endothelial cell dysfunction are likely to be more susceptible to the development of IFS due to compromised fluid movement out of the corneal stroma, thus facilitating the accumulation of fluid beneath the LASIK flap.18, 19, 20, 21

Finally, pressure-induced interlamellar stromal keratitis is an important sight-threatening interfacial complication after LASIK. This entity can occur either in the early postoperative period or as late as several months after the procedure.²² It is unusual for PISK to present as late as 10 years after the procedure, and we hypothesized that intraepithelial ingrowth created a fistula, creating a “space” that facilitated the entrance of fluid towards the LASIK interface. Lee et al. reported an interesting case of a post-LASIK patient presenting with PISK 9 years after the procedure, where the patient had a history of HLA-B27 negative spondyloarthropathy, the patient had an episode of uveitis and steroids were added to the treatment and PISK developed, and the clinical course improved after reduction of the steroid.²³

4. Conclusions

Refractive surgeons should recognize these similar entities, consider them as differential diagnoses, and indicate appropriate management. Usually, PISK is known as an early postoperative complication; however, in this report, we describe the first case of PISK 10 years after LASIK surgery associated with epithelial ingrowth, which is the latest onset reported in the literature (to the knowledge of the authors).

Funding

There is no funding received for this work.

Patient consent

The patient provided written consent regarding the publication of the present case report.

Acknowledgments and disclosures

No funding or grant support

Conflicts of interest:none.

All authors have no financial disclosure.

All authors attest that they meet the current ICMJE criteria for Authorship.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.