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ABSTRACT
DLK has been triggered by epithelial abrasions, trauma, and uveitis months and years after LASIK
8,9.
This is a unique case in which a gentleman developed aggressive DLK after CK over three years postLASIK.
CASE REPORT
I.
Case History
A. Patient demographics:
1. 48 Year old Caucasian gentleman.
B. Chief Complaints:
1. Decreased visual acuity after conductive keratoplasty
C. Ocular / Medical History:
1. High myope OD, OS. Excellent systemic health. Non-diabetic. No Autoimmune
pathology.
II. Pertinent Findings
A. Clinical:
1. Pre - LASIK refraction in his dominant right eye was -9.25+0.50x175. He
underwent microkeratome LASIK in that eye in 2004 and became hyperopic with a
refraction of +1.25+0.25x021 and an uncorrected acuity of 20/30-2. His left eye,
which had also undergone myopic LASIK was close to emmetropia with an
uncorrected acuity of 20/25+2. In September 2007, the uncorrected visual acuity
in the right eye was 20/30-2. Because of poor distance acuity in the right eye, the
patient desired an enhancement. Central pachymetry of that eye was 411µ.
Because of a concern of additional stromal tissue removal with additional excimer
laser ablation, the patient elected to proceed with a CK enhancement to treat his
hyperopia. One day post-CK, the distance uncorrected visual acuity was 20/50 and
pinholed to 20/20. Slit lamp examination revealed a clear cornea, and a well
positioned bandage contact lens. He was then informed of all post-operative
precautions and asked to return the next day for bandage contact lens removal.
2. On postoperative day 2, uncorrected visual acuity was 20/60 and pinholed to
20/30. Slit lamp examination revealed stage I DLK nasally. The patient was asked
to discontinue flouromethalone and use prednisolone acetate 1% Q1 hour, and
continue gatifloxacin 0.3% QID.
3. On postoperative day 3, uncorrected visual acuity was 20/25. Slit lamp
examination revealed significant progression as DLK moved into the interface with
clumping of cells. It was now at stage III.
III.Differential Diagnosis
A. Primary / leading:
1. Meibomian gland debris
2. Farinata
3. Flap edema
IV. Diagnosis and Discussion
A. DLK has been observed in eyes with previous LASIK after trauma, epithelial defects,
recurrent erosion, and uveitis. However, there have been no reported cases of DLK
occurring under the LASIK flap after CK. Given that epithelial defects are induced over
the CK spots, it is reasonable to postulate that it is this trauma to the corneal surface
that initiates the inflammatory response. To date, a singular definitive etiology of DLK
has not been identified. Rather, any form of debris in the lamellar interface may
activate DLK. This includes meibomian gland debris, red blood cells, fine sponge fibers,
metallic particles, wax from the microkeratome blade, or femtosecond energy.
Regardless of the DLK trigger, it is thought to be a sterile, immune-mediated
inflammatory process. Shah et al found that the presence of an epithelial defect of any
size after LASIK increased the relative risk of developing DLK by 24 times 8. The size of
the defect did not determine the density of the immune response in this study. Wilson
et al established that injured epithelium results in release of cytokines expressed by
stromal keratocytes and have described interleukin-1 (IL-1) as a “master trigger” of
the wound healing response in reaction to tissue injury10. This release of IL-1 has been
presented as one pathway to DLK development. Another is chemotaxis of
polymorphonuclear (PMN) leukocytes by epithelial growth factors8.
V. Treatment and Management
A. Treatment and Response to treatment:
1. After a thorough discussion regarding DLK and the need to prevent stromal
melting, the LASIK flap was lifted and the interface irrigated. The patient was
instructed to continue to use prednisolone acetate 1.0 % suspension Q1 hour and
gatifloxacin 0.3% QID.
2. Day four Post CK and One day after irrigation, the distance uncorrected visual
acuity was 20/30+2. The interface was significantly improved with fewer stromal
cells and the patient was instructed to decrease the frequency of prednisolone
acetate 1% to Q2 hours.
3. Day five Post CK - two days after irrigation the distance uncorrected visual acuity
was 20/30-2. The cornea was completely clear and the patient was instructed to
taper off the prednisolone acetate 1% over a two week period.
4. One month Post CK - one month after CK, the uncorrected visual acuity was 20/20
at distance and J5 at near. The patient reported being comfortable with his level of
correction at distance and near. The cornea remained clear without any
inflammatory cells or interface haze.
B. Bibliography:
1. McDonald MB, Durrie D, Asbell P, Maloney R, Nichamin L. Treatment of Presbyopia
with Conductive Keratoplasty. Six Month Results of the 1-Year United States FDA
Clinical Trial. Cornea 2004;23:661-668.
2. Comaish I, Lawless MA. Conductive Keratoplasty to Correct Residual Hyperopia
After Corneal Surgery. J Cataract Refract Surg 2003;29:202-206.
3. Hoffman RS, Fine H, Packer M. Incidence and Outcomes of LASIK with Diffuse
Lamellar Keratitis Treated with Topical and Oral Corticosteroids. J Cataract Refrac
Surg 2003;29:451-456.
4. Buhren J, Baumeister M, Kohnen T. Diffuse Lamellar Keratitis after Laser In Situ
Keratomileusis Imaged by Confocal Microscopy. Ophthalmology 2001;108:10751081.
5. Smith RJ, Maloney RK. Diffuse Lamellar Keratitis. A New Syndrome in Lamellar
Refractive Surgery. Ophthalmology 1998;105:1721-1726.
6. Linebarger EJ, Hardten DR, Lindstrom RL. Diffuse Lamellar Keratitis: Diagnosis and
Management. J Cataract Refract Surg 2000;26:1072-1077.
7. Godinich AG, Tex H, Steinert RF, Wu HK. Late Occurrence of Diffuse Lamellar
Keratitis After Laser In Site Keratomileusis. Arch Ophthalmology 2001;119:10741076.
8. Shah MN, Misra M, Wihelmus KR, Koch DD. Diffuse Lamellar Keratitis Associated
with Epithelial Defects after Laser In Situ Keratomileusis. J Cataract Refrac Surg
2000;26:1312-1318.
9. Jeng BH, Stewart JM, McLeod SD, Hwang DG. Relapsing diffuse Lamellar Keratitis
After Laser In Situ Keratomileusis Associated With Recurrent Erosion Syndrome.
Arch Ophthalmology 2004;122:396-398.
10. Wilson SE, Liu JJ, Mohan RR. Stromal-epithelial interactions in the cornea. Progr
Retin Eye Res 1999;8(3):293-309.
VI. Conclusion
A. This case underscores the importance of careful early post-operative examination and
follow up when CK is performed over a LASIK flap. The potential for inflammation
should be considered and a careful examination for development of DLK is critical in
order to lift and irrigate the flap at the appropriate time. A relatively unstudied aspect
of treatment of the epithelial defect is the impact of the bandage contact lens on the
inflammatory cellular cascade. We suggest that the bandage contact lens likely
decreased the localized inflammatory response by simply helping the defect heal.
Lifting and irrigating the flap while carefully guarding against introduction of epithelial
cells into the interface is also important. While there are distinct advantages to using a
hyperopic enhancement tool after LASIK in order to preserve corneal biomechanical
strength, surgeons should be aware of this rare but serious complication.
Nevertheless, diligent postoperative follow-up and treatment can avoid potential for
any visual compromise.