CASE PRESENTATION
In November 2006, a 30-year-old female underwent LASIK with the Hansatome 160/8.5 (Bausch & Lomb, Rochester, New York) and the Allegretto Wave Eye-Q (WaveLight AG, Erlangen, Germany) for a -5.50 OD and -6.00 D OS (Figures 1 and 2).

Several days postoperatively, the patient presented with severe diffuse lamellar keratitis (DLK), which was treated with irrigation. The surgeon then diagnosed the patient with striae and suggested that the DLK was resolving.

Ten days postoperatively, the patient was evaluated, and her UCVA was 20/25 and 20/60 pinhole: NI and 20/30. At this point, she was using prednisolone acetate 1% every other hour as well as other lubricants. Significant striae and interface edema were also found in a localized area of approximately 1 mm diameter paracentral OD and central in the OS cornea (Figure 3). Intraocular pressure was 15 to 19 mm Hg in both eyes measured in the center, paracentral, and outside the flap cornea.

What would be the next step in managing this very unhappy patient?

MICHAEL ASSOULINE, MD, PhD
As noted in the slit-lamp photos, this patient most likely has bilateral stage four DLK that has collected in the center of the interface. This patient appears to have a good light reflex from the epithelium at the slit lamp. Still, I would pay close attention to the epithelial status and potential toxicity of topical medications during follow-up.

The irregular astigmatism observed on the Pentacam (Oculus Optikgerate GmbH, Wetzlar, Germany) curvature maps (ie, pseudocentral island, small optical zone, slight decentration, marked peripheral steepening) seems to result mainly from the interface edema. I hypothesize that the patient's visual limitation is related to residual interface edema, resulting striae, and incipient flap damage (eg, infiltrate, melting) from severe inflammation. Because there cannot be scarring at this stage, there is no indication of flap malposition.

If that is the case, I recommend tapering the steroid treatment to eight times daily for 4 days, six times daily for 4 days, three times daily for 8 days, and once daily for 8 days before discontinuing the topical steroid. This may occur once it is ascertained that the DLK has resolved.

The flap and interface edema—which translate into severe paracentral striae (on slit-lamp examination) and irregular astigmatism with nasal steepening in OD and upper steepening in OS (on Pentacam curvature maps)—may resolve over a couple of months. This resolution would allow for a better assessment of flap damage, which was a consequence of inflammation-induced flap melting.

Persistent striae after the resolution of interface edema would indicate flap malpositioning and scarring. It would require flap stretching. I do not favor hypotonic solutions, epithelial removal, or sutures. Instead, I use two dry microsponges to firmly stretch the back surface of the flap over the adjacent upper sclera. In case of late stretching (ie, 1 month postoperatively or later) I also perform a 10 µm deep, 9 mm diameter phototherapeutic keratectomy (PTK) ablation of the back surface of the flap. This helps to break the collagen and cellular bridges that may hold the flaps together.

At 3-month follow-up, I usually advise a patient with a previous severe DLK episode and irregular astigmatism from stromal loss (either from the flap or the bed) to have a rigid gas-permeable contact lens fitted by an experienced contact lens specialist. This lens should be worn for at least 1 year to allow for a complete resolution of inflammation and wait for spontaneous corneal remodeling. The contact lens is a great tool for restoring the patient's vision and confidence; it avoids the premature need for more invasive and hazardous management methods.

One year postoperatively, I would evaluate the residual refraction and stromal and flap thickness using ultrasound pachymetry, ultrasound biomicroscopy, Visante Optical Coherence Tomographer (OCT; Carl Zeiss Meditec AG, Jena, Germany), and a custom anterior segment Zeiss OCT (Carl Zeiss Meditec AG).

I would also evaluate the residual irregular astigmatism using Orbscan elevation topography and a ZyWave aberrometer (both manufactured by Bausch & Lomb).

These data are essential for determining the correction by means of careful flap dissection and lifting followed by wavefront- or topography-guided ablation, if there is sufficient flap thickness and residual stroma present.

Ablating the spherical component of the correction from the back surface of the flap and cylinder and components of higher-order aberration from the stromal bed is a good option. This may help remove some scar tissue from both sides of the interface and save the stromal bed. If the cornea appears too thin (ie, less than 380 µm), I would advise the patient to delay more invasive approaches (ie, automated or deep anterior lamellar keratoplasty) for several years, to allow for spontaneous remodeling of the corneal surface. This is often amazingly efficient!

Compassion, in-depth explanations, patience, and the support of a seasoned contact lens specialist, are essential to retain the patient's trust and limit legal developments.

MIRKO R. JANKOV II, MD, PhD
Significant striae decrease vision quality and may negatively impact a patient's UCVA and BCVA. If this occurs, it is necessary to immediately relift and reposition the flap.

On the other hand, DLK (ie, stage three or higher), considerably decreases visual acuity and prompts immediate action to stop the permanent scarring that occurs in the progression of DLK to stage four. It seems, considering this patient's history, that she had been treated for stage three DLK, but the flap was inadequately repositioned postoperatively. At this moment, the patient apparently presents stage four DLK with paracentral scarring in addition to folds and striae; it was worse in the OD. Pentacam examination photos confirm an irregular anterior corneal shape. Considering that scattering is the underlying principal (Scheimpflug) of this examination technique, however, one should be reserved when analyzing the results. In this case, both front- and backscatter are significantly increased by the present scar; this would render the anterior cornea contour suspicious and create an inaccurate back surface image. That fact, in turn, also invalidates the pachymetry maps.

A better indicator of the true anterior surface would be a corneal topography based on placido rings, while the pachymetry should be reconfirmed by ultrasound contact pachymetry; it is expected to be considerably thicker than 315 µm OD and 334 µm OS, as measured with Pentacam.

Considering the striae that are present in the pupillary area past 9 months postoperative, it seems reasonable to believe that the flap should be repositioned with additional near-horizontal sutures, perpendicular to the line of the fold. Epithelial removal may be necessary to perform extensive ironing of both stromal bed and the flap itself. Because of the length of time since the original surgery, however, I do not believe that it is likely that the striae will completely resolve.

Haze, a grainy appearance of the stromal bed, and the corresponding part of the flap should be expected with DLK. If the scar is more pronounced on the stromal bed, limited PTK can be performed with masking fluid to partially remove the scar and improve the optical quality of this cornea.

Topography-guided PTK over the flap is not indicated until the striae, as well as the interface scar, have been significantly reduced. This would eliminate the optical cause of the reduced quantity and quality of vision and render results when changing the shape of the cornea with the aid of a topography-guided excimer laser.

WALTER SEKUNDO, MD
This patient exhibits typical problems associated with flap relift, particularly when accompanied by DLK, striae, and an irregular topography. Because it has been 10 days after the primary surgery, the irregular anterior floats in the photos represent, at least in part, the localized edema. The first measure for treatment, therefore, is to decide whether the DLK is truly resolving or is actually an infectious interface keratitis. I would follow this patient daily and keep her on hourly topical steroids.

If the clinical picture does not deteriorate over a few days, I may consider adding oral steroids to the treatment. If the clinical picture suggests any deterioration of the condition, however, I would relift and take smears from both the stromal section of the flap and stromal bed.

Assuming that the DLK has resolved, I would expect the topography to regularize and the visual acuity to increase. If this does not occur within 7 to 10 days, further surgical intervention is justified, as flap wrinkles become the most possible cause of poor vision. In that case, relifting with epithelial removal over affected areas, hydrostretching and, possibly, a temporary torque-antitorque 10-0 nylon flap suture should be attempted. This will ensure striae are removed from the visual axis. Steroids should be topped-up, if an epithelial debridement was carried out.

I am somewhat concerned about the possibility of ectasia in the long run, because Pentacam shows the thinnest points of the cornea measure 315 µm and 334 µm. Assuming that a 160-µm Hansatome head usually cuts roughly 150-µm flaps, the residual stromal bed is 165 µm OD and 184 µm OS! The posterior elevation of +40 increases my concerns of the upcoming corneal ectasia in this patient.

Michael Assouline, MD, PhD, is in practice at the Clinique de La Vision, in Paris. Dr. Assouline states that he is a consultant for Bausch & Lomb and has no direct financial interest in the company or products mentioned in this article. He is a member of the CRST Europe Editorial Board. He may be reached at +33 1 45 56 92 92; ma@inclo.com.

Mirko R. Jankov II, MD, PhD, is an ophthalmologist at Milos Eye Hospital, Medical Academy in Belgrade, Serbia. Dr. Jankov states that he is paid consultant for WaveLight AG. He may be reached at tel: +381 11 245 5759; fax: +381 11 243 7503; or mirko.jankov@milosklinika.com.

Walter Sekundo, MD, is Professor of Ophthalmology and Deputy Chairman, at the University Eye Hospital of Mainz, Germany. Professor Sekundo states that he receives research support and travel reimbursements from Carl Zeiss Meditec AG. He may be reached at sekundo@augen.klinik.uni-mainz.de.

A. John Kanellopoulos, MD, is Director of Laservision Eye Institute, in Athens, Greece. He is Attending Surgeon for the Department of Ophthalmology at the Manhattan Eye, Ear, & Throat Hospital, in New York and Clinical Associate Professor of Ophthalmology at New York University Medical School. Dr. Kanellopoulos states that he has no financial interest in the products or companies mentioned. He is a member of the CRST Europe Editorial Board. Dr. Kanellopoulos may be reached at +30 21 07 27 27 77; laservision@internet.gr.

Jérôme C. Vryghem, MD, is from the Brussels Eye Doctors in Brussels, Belgium. Dr. Vryghem states that he has no financial interest in the products or companies mentioned. Dr. Vryghem is a member of the CRST Europe Editorial Board. He may be reached +32 2 741 69 99; j.c.vryghem@vryghem.be.