DLK (Diffuse Lamellar Keratitis)

A case of late-onset diffuse lamellar keratitis 12 years after laser in situ keratomileusis.
Kamiya K, Ikeda T, Aizawa D, Shimizu K.
Jpn J Ophthalmol. 2010 Mar;54(2):163-4.

Excerpt:

We present herein a case of DLK with an extremely delayed onset, occurring 12 years after LASIK, necessitating intensive steroidal treatment to avoid subsequent visual disturbances....

There have been several reports of late-onset DLK after lamellar surgery, but these cases occurred within 3 years of surgery... In the present study, we found epithelial ingrowth after treatment, indicating incomplete flap integrity at its edge...

In summary, this case report indicates that LASIK can cause DLK as late as 12 years postoperatively, which also emphasizes the importance of long-term follow-up after this surgery. Refractive surgeons should be held responsible for post-LASIK patients not only in the early but also in the late postoperative period, since this postoperative complication can be resolved with minimal sequelae if diagnosed in a timely fashion.

Confocal Microscopy Comparison of IntraLase Femtosecond Laser and Moria M2 Microkeratome in LASIK.
Journal of Refractive Surgery Vol. 23 No. 2 February 2007.
Jaime Javaloy, MD, PhD; María T. Vidal, MD, PhD; Ayman M. Abdelrahman, MD; Alberto Artola, MD, PhD and Jorge L. Alió, MD, PhD.

Excerpt:

"Diffuse lamellar keratitis consists of a multi-etiologic syndrome that expresses variable degrees of inflammation at the interface of eyes operated by LASIK.37,38 As DLK after LASIK using a femtosecond microkeratome has not been reported previously, the 17% prevalence rate of this syndrome (even considering that just 6.25%—1 case—was greater than grade I or II) in our series has to be taken into account."

Journal of Refractive Surgery Volume 17 May/June 2001
Complications of Laser in situ Keratomileusis: Etiology, Prevention, and Treatment
Renato Ambrósio Jr, MD; Steven E. Wilson, MD

Excerpts:

Smith and Maloney thoroughly described diffuse lamellar keratitis (DLK) (American Academy of Ophthalmology, San Francisco, CA, November, 1997).71 Other reports have appeared since that time (Linebarger EJ. Diffuse lamellar keratitis: trouble in paradise? ASCRS Film Festival, Grand Prize Winner, 1999).20,41,72-78 It has also been called sands of the Sahara syndrome (Bobby Maddox, MD, El Paso, TX, coined the phrase), because of the characteristic wavy appearance at slit-lamp examination.

In severe cases, it is associated with stromal necrosis and irregular astigmatism.

However, we have seen two cases of infectious keratitis in which treatment was inappropriately delayed because of erroneous diagnosis of DLK. Both cases had severe vision loss.

The incidence of DLK is highly variable. One report noted an incidence of approximately 1 in 500.74 Some high volume LASIK surgeons have reported never seeing a case in their own practice. We have seen only two mild cases in 3000 LASIK procedures. Others have experienced focal outbreaks of DLK that have included dozens of patients.

Another grading system has been proposed by Linebarger (Linebarger, 1999, cited above).75 Stage 1 DLK is typically seen on day 1 postoperatively as white, granular cells in the periphery with sparing of the visual axis. Stage 2 Typically seen on postoperative day 2 or 3, shows white cells in the visual axis.
Stage 3 DLK involves an aggregation of cells clumped in the visual axis and associated with haze
and reduced vision. Stage 4 Involves central stromal necrosis, melt, and secondary hyperopia with irregular astigmatism.

At the other extreme, severe (grade 4) cases typically have decreased vision and severe pain associated with marked interface inflammation and necrosis that results in topographic flattening of the corneal contour, secondary irregular astigmatism, and poor vision.

Many potential etiologies for DLK have been proposed (Linebarger, 1999, cited above).75-77 Most of these are based on speculation without supporting data. These have included betadine from surgical preps, impure balanced salt solution, retained meibomian secretions and other tear film components, metallic debris, use of improper detergents, talc from gloves, thermal effects from the excimer laser, lubricants on the microkeratome or blades, topical medications such as anesthetics, bacterial cell wall hypersensitivity, and biofilms from inadequate sterilization protocols.

The bacterial cell wall hypersensitivity mechanism could have been the underlying factor in a recent epidemic of DLK.77 The authors suggested that the microkeratome or irrigating cannula became contaminated by bacteria. These bacteria may reside in water left standing in the sterilizer. If the contaminated instruments are cleaned and left to dry, bacteria could proliferate on residual trace protein and the bacterial cell count could increase significantly.

These data suggest that injury to the surface epithelium or epithelial debris left within the LASIK interface triggers production of factors that are chemotactic for inflammatory cells via interleukin-1 release. This mechanism could account for many DLK cases.

Surgical technique may limit DLK, whatever the underlying mechanism.

Eyes with severe DLK are at high risk for stromal necrosis that may be focal and result in haze, irregular
astigmatism, and hyperopic shift.