Despite the absence of visible preoperative abnormality, the behavior of the epithelium at the time of microkeratome flap creation suggests the patient has significant anterior basement membrane dystrophy.
In the right eye, the postoperative epithelial defects are located inferiorly and probably contributed to the recurrence of the epithelial ingrowh into the interface. Although there was no visible ingrowth until 10 months postoperatively by history, the topography at 2 weeks (Figure 2, left) shows inferior flattening consistent with epithelial ingrowth or edema that may be secondary to poor epithelial integrity. At the 18-month examination, the topography remains mildly irregular, but there is less flattening in the inferior zone. This is consistent with reasonable UCVA and a normal BCVA of 20/20 accompanied by a minimal refractive error.
Although the cystic epithelial ingrowth in the interface in Figure 1, left, is impressive at 18 months, I would not relift the flap at this time as it would disturb the surface epithelium again. This might lead to recurrence of epithelial ingrowth that is even more extensive. The indications for flap lifting and cleaning the interface are optical distortion or melting of the overlying flap. Neither is present. The right eye should continue to be observed carefully at frequent intervals and the extent of epithelial ingrowth monitored by direct measurement and sequential corneal topography.
The visual acuity in the left eye is reported to have dropped to 20/100 without improvement with spectacles. No further information is given on the physical findings or diagnostic measurements. A thorough evaluation of all possible causes of decreased acuity is appropriate. For this discussion, I will assume the anterior and posterior segments are normal with the exception of the cornea. Assuming that visual acuity normalizes with a rigid contact lens refraction, the determination must be made whether the irregularity of the surface epithelium and basement membrane is responsible for the fairly profound loss of acuity or whether other factors are causing irregular astigmatism. The inability of the topographer to capture a printable image strongly suggests there is major disruption of the epithelium. If so, I would initially debride the defective epithelium, place a bandage soft contact lens, and institute an intensive prophylactic steroid and antibiotic regimen. The steroid can be tapered once the risk of recurrent DLK passes. The bandage soft contact lens should be left for an extended period, at least 1 month if possible.
Underlying contributing factors to the epitheliopathy must be investigated. The inferior location suggests there may be an element of dry eye, lagophthalmos, or both. In addition to intensive topical lubrication during the day and a gel or ointment at bedtime, lid taping during sleep may prove beneficial if nocturnal lagophthalmos is present. Strong consideration should also be given to placement of punctal plugs, even if Schirmer testing is normal, to increase the retention of adequate tear film.
If the epithelium continues to break down on a recurrent basis, PTK may be helpful. I have had excellent results in establishing good epithelial adhesion with PTK for anterior basement membrane dystrophy, not only in untreated corneas but also in patients with LASIK flaps. After manual debridement, excimer laser pulses are applied to achieve approximately 5 μm of tissue removal (typically no more than 20 pulses in any given area). This is usually done with a broad-beam laser. This minimal amount of tissue removal has not triggered clinical haze in the small number of patients who have required PTK after LASIK. However, stable reepithelialization has been achieved in each of these challenging patients.