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Clinicopathologic Reports, Case Reports, and Small Case Series
July 2001

Late Occurrence of Diffuse Lamellar Keratitis After Laser In Situ Keratomileusis

Arch Ophthalmol. 2001;119(7):1074-1076. doi:

Diffuse lamellar keratitis (DLK) is a noninfectious inflammatory complication associated with laser in situ keratomileusis (LASIK).1 Post-LASIK sterile interface keratitis has also been described as "sands of the Sahara syndrome" and "central focal interface opacity after LASIK."2,3 The corneal infiltrates may be focal or multifocal but remain confined to the lamellar interface without extension, anterior chamber reaction, or associated epithelial defect. Common to all previously reported cases is an onset within 1 month after LASIK treatment, enhancement, or flap manipulation.14 We report 2 cases of DLK appearing after the immediate postoperative period (2-7 months after LASIK), 1 of which had bilateral involvement.

Report of Cases
Case 1

A 48-year-old woman with euthyroidism and a treatment history of hypothyroidism underwent bilateral sequential LASIK using a 180-µm Hansatome microkeratome (Bausch and Lomb, Rochester, NY) and a Summit Apex Plus excimer laser (Summit Technology, Waltham, Mass). Preoperative refraction of −4.75 +1.50 × 092 OD and −4.50 +1.75 × 085 OS yielded a best-corrected visual acuity of 20/20 OU. Fifty percent epithelial flap defects in both eyes and mild DLK in the left eye were present on postoperative day 1. The defects healed with bandage soft contact lens wear and the DLK resolved after 1 week of intensive fluorometholone treatment. One month postoperatively, uncorrected visual acuity was 20/40 OD and 20/30 OS. Refraction of +0.25 +1.50 × 102 OD and −0.75 +0.75 × 037 OS yielded a best-corrected visual acuity of 20/25 OU. The flaps were well healed with the exception of mild interpalpebral punctate epithelial staining in both eyes. She was offered bilateral lower punctal plugs, which she declined.

Two months postoperatively she complained of a sudden onset of redness and a foreign body sensation in her left eye. Examination was remarkable for an uncorrected visual acuity of 20/40 OS. Slitlamp biomicroscopy showed minimal diffuse conjunctival hyperemia and a focal 2 × 2-mm nonsuppurative infiltrate in the lamellar interface inferocentral to the pupil. Mild edema of the flap without epithelial defects was noted. The anterior chamber was quiet. A regimen of hourly topical ofloxacin was started. Examination 24 hours later revealed a visual acuity of counting fingers. Slitlamp biomicroscopy showed severe diffuse conjunctival hyperemia, diffuse stromal edema with a large central epithelial defect, and a diffuse lamellar infiltrate without anterior or posterior extension (Figure 1). The lamellar flap was lifted and debrided of soft infiltrate. Scrapings were sent for aerobic, anaerobic, atypical mycobacterial, and fungus staining and culturing. The interface was irrigated with fortified vancomycin and tobramycin eye drops, the flap was repositioned, and the bandage soft contact lens was applied. Fortified vancomycin and tobramycin eye drops were administered hourly. One day later, discrete granular infiltrates reappeared in the interface. Stains and cultures revealed no organisms. Topical prednisolone acetate was given every 2 hours to treat DLK and then hourly when cultures remained without growth after 48 hours. On complete reepithelialization, the bandage soft contact lens was removed and the dose of fortified antibiotics was decreased to 4 times per day. Prednisolone was taken hourly. On day 21, uncorrected visual acuity was 20/60 OS. Refraction of plano +1.00 × 180 yielded a best-corrected visual acuity of 20/30 OS. Slitlamp biomicroscopy showed mild interface scarring centrally, 2+ granular infiltrates, and 1+ stromal flap edema (Figure 2).

Figure 1.
Patient 1, left eye, 2 months
postoperatively. Slitlamp biomicroscopy reveals severe lamellar keratitis
with diffuse stromal edema, overlying epithelial defect, and diffuse lamellar
infiltrate without anterior or posterior extension. Visual acuity is counting
fingers.

Patient 1, left eye, 2 months postoperatively. Slitlamp biomicroscopy reveals severe lamellar keratitis with diffuse stromal edema, overlying epithelial defect, and diffuse lamellar infiltrate without anterior or posterior extension. Visual acuity is counting fingers.

Figure 2.
Patient 1, left eye, 3 weeks after
treatment. Slitlamp biomicroscopy shows organized healing of interface keratitis.
Visual acuity is 20/30 OS with refraction of plano +1.00 × 180.

Patient 1, left eye, 3 weeks after treatment. Slitlamp biomicroscopy shows organized healing of interface keratitis. Visual acuity is 20/30 OS with refraction of plano +1.00 × 180.

The left eye remained stable during the prednisolone dose taper. However, 3 months postoperatively, her right eye showed a small epithelial erosion without keratitis. On follow-up day 3, slitlamp biomicroscopy of the right eye revealed a healing erosion with few focal interface opacities and mild diffuse granular infiltrates (Figure 3). The keratitis resolved after a 5-day regimen of prednisolone acetate taken hourly and ofloxacin taken 4 times per day.

Figure 3.
Patient 1, right eye, 3 months
postoperatively. Slitlamp biomicroscopy shows mild lamellar keratitis with
few focal interface opacities and mild granular infiltrates centrally.

Patient 1, right eye, 3 months postoperatively. Slitlamp biomicroscopy shows mild lamellar keratitis with few focal interface opacities and mild granular infiltrates centrally.

Case 2

A 51-year-old woman with myopic amblyopia currently taking thyroxine for hypothyroidism underwent bilateral LASIK for treatment of high myopia. She came for a second opinion regarding management of superior limbal keratoconjunctivitis in the right eye 7 months postoperatively. Refraction of −1.75 yielded a visual acuity of 20/40 OD. Slitlamp biomicroscopy was remarkable for mild superior conjunctival hyperemia, redundancy, and rose Bengal staining. She underwent superior conjunctival resection and was given tobramycin/dexamethasone ointment to apply 4 times per day. Three days after resection, she complained of worsening pain and decreased vision. On examination, her best-corrected visual acuity was 20/80 OD. The superior conjunctival defect was healing well without suppuration. Diffuse granular infiltrates were visible in the flap interface without epithelial defects or anterior chamber reaction. Her regimen was switched to ofloxacin taken 4 times per day and prednisolone acetate taken hourly. Follow-up examination 48 hours later showed best-corrected visual acuity to be 20/40 OD with completely resolved interface keratitis.

Comment

The causes of DLK are not clearly defined. A rare postoperative complication of LASIK, with an estimated incidence of 3 in 400,2 DLK is thought to be a secondary inflammatory response to a variety of potential agents within the space of the flap interface. Four clinical stages have been described, ranging from non–visually significant focal infiltrates to diffuse infiltrates with stromal necrosis.5 Known to occur within a week after either primary LASIK or enhancement procedures, DLK has also been reported after epithelial flap debridement to reduce visually significant basement membrane irregularities 1 month after LASIK enhancement.4

Unusual in our cases is the late onset of DLK. In the most severe case, the lack of initial epithelial defect, confinement of infiltrate to the interface, rapid progression despite hourly ofloxacin treatment, rapid improvement with intensive topical steroids, and negative microbiology culture results strongly support a diagnosis of DLK rather than infectious keratitis. One case series review of infectious ulcerative keratitis following LASIK reported that all cases had epithelial defects and none had infiltrate confined only to the interface.6 Our case 1 had documented recurrent epithelial erosions and typical DLK in the acute postoperative period. Case 2 had probable microdisruption of the superior corneal epithelium after manipulation of the superior conjunctiva. We propose a mechanism whereby an inflammatory reaction to corneal surface disruption occurs in the potential space of the flap interface resulting in a clinical picture of lamellar keratitis.

We report these 2 cases to bring attention to the possibility of DLK occurring beyond the immediate postoperative period, especially when the potential for corneal surface disruption exists. As more patients undergo LASIK, more cases of late-onset DLK will be seen. Care must be taken to exclude infectious keratitis. However, the prognosis for recovery is good following intensive topical steroid treatment.

supported in part by a grant from the Heed Ophthalmic Foundation, Cleveland, Ohio (A.C.G.).

The authors have no proprietary interest in any of the companies mentioned. Dr Steinert is a paid consultant for Summit Technology.

Corresponding author and reprints: Helen K. Wu, MD, Refractive Surgery Center, Tufts University School of Medicine, New England Eye Center, 750 Washington St, Box 450, Boston, MA 02111 (e-mail: helenkw@aol.com).

References
1.
Smith  RJMaloney  RK Diffuse lamellar keratitis: a new syndrome in lamellar refractive surgery. Ophthalmology. 1998;1051721- 1726Article
2.
Kaufman  SCMaitchouk  DYChou  AGY  et al.  Interface inflammation after laser in situ keratomileusis: sands of the Sahara syndrome. J Cataract Refract Surg. 1998;241589- 1593Article
3.
Fraenkel  GECohen  PRSutton  GL  et al.  Central focal interface opacity after laser in situ keratomileusis. J Refract Surg. 1998;14571- 576
4.
Steinert  RFMcColgin  AZWhite  A  et al.  Diffuse interstitial keratitis after laser in situ keratomileusis: a nonspecific syndrome. Am J Ophthalmol. 2000;3380- 381Article
5.
Machat  JJ LASIK complications. Machat  JJSlade  SGProbst  LE eds. The Art of LASIK. 2nd ed. Thorofare, NJ Slack Inc1999;392- 396
6.
Quiros  PAChuck  RSSmith  RE  et al.  Infectious ulcerative keratitis after laser in situ keratomileusis. Arch Ophthalmol. 1999;1171423- 1427
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