From the Department of Ophthalmology, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Cheng-Kuo Cheng, MD, Department of Ophthalmology, Shin-Kong Wu Ho-Su Memorial Hospital, No. 95, Wen-Chang Road, Shih-Lin District, Taipei 11120, Taiwan.
Pressure-induced interface keratitis, which was first reported by Belin et al., resembles diffuse lamellar keratitis in appearance but is associated with elevated intraocular pressure (IOP) and is exacerbated by steroid treatment.1,2 Most reported cases of pressure-induced interface keratopathy were after laser in situ keratomileusis (LASIK) in patients suffering increased IOP associated with topical steroid therapy. In this report, we present a clinically distinctive form of pressure-induced interface keratopathy that occurred following a pars plana vitrectomy with intraocular gas tamponade for repair of a macular hole 8 years after a LASIK procedure.
A 35-year-old woman underwent LASIK in both eyes in 2000. A corneal flap was created with a superior hinge using a Hansatome microkeratome (Bausch & Lomb, Rochester, NY) with an 8.5-mm suction ring. After the corneal flap was lifted, the corneal stromal bed was ablated with an excimer laser (Technolas 217z; Bausch & Lomb). The optical and transitional zones were 5.6 and 6.8 mm, respectively, and there were no complications. A superficial punctate keratopathy was noted in the right eye 1 week later and improved after 2 weeks of treatment with lubrication. The best-corrected visual acuity was 6/6.7 in each eye with normal IOP at that time.
The patient had regular follow-up over the next 8 years. An incomplete posterior vitreous detachment with apparent vitreomacular traction of her right eye was noted 1 year later, which caused a mild decrease of best-corrected visual acuity to 6/8.6. The condition remained stable until 2008, when a macular hole developed in her right eye. Pars plana vitrectomy and intraocular gas tamponade with 10% C3F8 were then performed without difficulty. Elevated IOP up to 37 mm Hg measured by a computerized non-contact tonometer (Advanced Logic Tonometer, Xpert NCT Plus 12450; Reichert Inc., Depew, NY) was noted 2 days after surgery, and a concurrent stage 2 diffuse lamellar keratitis-like interface infiltration and opacity were also found during silt-lamp examination (Figs. A and B). She complained of pain, blurred vision, a foreign body sensation, and sensitivity to light. Because pressure-induced interface keratopathy was highly suspected, the anti-inflammatory agent (prednisolone acetate 1%) was discontinued and antiglaucomatous agents (0.5% timolol maleate and oral acetazolamide) were prescribed. The interface infiltration resolved spontaneously after the IOP decreased to 11 mm Hg 2 days later (Figs. C and D).
Figure. (A) Pressure-Induced Interface Keratopathy and Interface Infiltration (arrowhead). (B) Margins of the Pressure-Induced Interface Keratopathy (arrows). (C and D) the Interface Infiltration Has Resolved After Control of the Intraocular Pressure.
Interface infiltration is a common complication of LASIK. The most commonly described presentation is diffuse lamellar keratitis. Diffuse lamellar keratitis was first reported in 1998 as diffuse noninfectious infiltrates confined to the interface accompanied by an inflammatory reaction that typically occurred the first week after LASIK surgery.3 Most cases of diffuse lamellar keratitis occur soon after the LASIK procedure.4 The cause and pathophysiology of diffuse lamellar keratitis is still poorly understood and no etiology is identified in most cases. Some reports revealed an increased incidence of diffuse lamellar keratitis in patients with corneal epithelial defects after surgery.5–7 Postoperative trauma has also played a role in diffuse lamellar keratitis.8,9 Recent studies have even suggested that some types of surgical marking pens may be toxic and could be a factor in causing diffuse lamellar keratitis.10,11
Pressure-induced interface keratopathy is another distinctive entity that presents with interface infiltration. Belin et al. first described 4 patients with pressure-induced stromal keratitis following LASIK in 2002.1 The infiltration of the interface, which occurred with increased IOP, resolved after IOP reduction and did not respond to topical steroids. Nordlund et al. termed the condition pressure-induced interface keratitis in 2004.2 They reported 10 eyes in 6 patients with late-onset interface infiltration and increased IOP on average 28 days after the LASIK procedure (range: 8 to 69 days). Lamellar infiltration was exacerbated by topical steroids and resolution did not occur until the IOP was controlled.
Our patient had interface infiltration and opacity 8 years after LASIK surgery with coexisting elevated IOP due to intraocular gas tamponade for the management of a macular hole. The infiltration responded to a reduction of IOP but not to topical steroid treatment. We believe our case was pressure-induced interface keratopathy rather than diffuse lamellar keratitis because the interface infiltration occurred very late, was associated with increased IOP, and responded to lowering of the IOP but not to steroid therapy, and because no other inflammatory or infectious causes were noted in the follow-up period.
It has been reported that IOP may be underestimated after LASIK because corneal thickness and rigidity are decreased after LASIK surgery.12,13 Different types of tonometry including Goldmann applanation tonometry, noncontact tonometry, Tono-Pen tonometry (Mentor, Santa Barbara, CA), and dynamic contour tonometry, are affected by different confounders such as the mean keratometric power, central corneal thickness, and lens thickness.14 In one study, computerized noncontact tonometry was not significantly associated with laser ablation depth.15 We also used computerized noncontact tonometry for the IOP measurements in our patient.
Because pressure-induced interface keratopathy may be worsened by topical steroids and elevated intraocular pressure, early recognition is important. Treatment consists primarily of normalizing the IOP and discontinuing topical steroids. Resolution of infiltration can usually be obtained by lowering the IOP, as demonstrated in our case.
Pressure-induced interface keratopathy is not a usual complication after LASIK, and therefore it may easily be missed in patients who have undergone LASIK several years before. We present this case to emphasize that elevated IOP may cause interface infiltration even up to 8 years after LASIK surgery. Surgeons are advised to be aware of pressure-induced interface keratopathy when performing surgery with intraocular gas tamponade in patients after LASIK. Assessment of intraocular pressure is essential in patients presenting with interface keratopathy, especially in patients undergoing posterior segment operations with intraocular gas tamponade.
- Belin MW, Hannush SB, Yau CW, Schultze RL. Elevated intraocular pressure-induced interlamellar stromal keratitis. Ophthalmology. 2002;109:1929–1933. doi:10.1016/S0161-6420(02)01163-6 [CrossRef]
- Nordlund ML, Grimm S, Lane S, Holland EJ. Pressure-induced interface keratitis: a late complication following LASIK. Cornea. 2004;23:225–234. doi:10.1097/00003226-200404000-00003 [CrossRef]
- Smith RJ, Maloney RK. Diffuse lamellar keratitis: a new syndrome in lamellar refractive surgery. Ophthalmology. 1998;105:1721–1726. doi:10.1016/S0161-6420(98)99044-3 [CrossRef]
- Linebarger EJ, Hardten DR, Lindstrom RL. Diffuse lamellar keratitis: identification and management. Int Ophthalmol Clin. 2000;40:77–86. doi:10.1097/00004397-200007000-00010 [CrossRef]
- Sachdev N, McGhee CN, Craig JP, Weed KH, McGhee JJ. Epithelial defect, diffuse lamellar keratitis, and epithelial ingrowth following post-LASIK epithelial toxicity. J Cataract Refract Surg. 2002;28:1463–1466. doi:10.1016/S0886-3350(02)01236-1 [CrossRef]
- Haw WW, Manche EE. Late onset diffuse lamellar keratitis associated with an epithelial defect in six eyes. J Refract Surg. 2000;16:744–748.
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- Weisenthal RW. Diffuse lamellar keratitis induced by trauma 6 months after laser in situ keratomileusis. J Refract Surg. 2000;16:749–751.
- Rosman M, Chua WH, Tseng PS, Wee TL, Chan WK. Diffuse lamellar keratitis after laser in situ keratomileusis associated with surgical marker pens. J Cataract Refract Surg. 2008;34:974–979. doi:10.1016/j.jcrs.2008.02.014 [CrossRef]
- Hadden OB, McGhee CN, Morris AT, Gray TB, Ring CP, Watson AS. Outbreak of diffuse lamellar keratitis caused by marking-pen toxicity. J Cataract Refract Surg. 2008;34:1121–1124. doi:10.1016/j.jcrs.2008.03.024 [CrossRef]
- Vakili R, Choudhri SA, Tauber S, Shields MB. Effect of mild to moderate myopic correction by laser-assisted in situ keratomileusis on intraocular pressure measurements with Goldmann applanation tonometer, Tonopen, and pneumatonometer. J Glaucoma. 2002;11:493–496. doi:10.1097/00061198-200212000-00007 [CrossRef]
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