CASE PRESENTATION
A 37-year-old white male presented with complaints of decreased vision after a motor vehicle accident involving the deployment of an airbag in December 1999. He had undergone an uncomplicated bilateral LASIK procedure for moderate myopia in March 1999. Postoperatively, the patient had a UCVA of 20/25 OD and 20/20 OS.
The fundus exam revealed a giant retinal tear with the macula off in the right eye and multiple horseshoe-shaped tears in the left eye. The patient subsequently underwent a laser retinopexy in the left eye and a scleral buckle procedure in the right eye. In May 2000, a recurrent retinal detachment of the right eye necessitated additional argon laser retinopexy. When a progressive retinal detachment occurred in the right eye later that month, a vitrectomy and lensectomy were performed and a C3F8 gas bubble placed. One month later, the retina in his right eye redetached, so the patient underwent repeat vitrectomy, membrane peeling, and placement of silicone oil.
The patient then developed rapid-onset band keratopathy within the LASIK flap of his right eye. Another ophthalmologist performed manual debridement. It is unknown whether EDTA chelation was also employed. During the next several months, the band keratopathy recurred. In October 2000, an additional surgical procedure was performed to remove more scar tissue from the retina and to fill the aphakic eye with silicone oil.
In May 2001, we saw the patient for an initial consultation. Slit lamp biomicroscopy revealed that the anterior chamber was filled with silicone oil and the posterior chamber was 90% full of silicone oil. The entire LASIK flap was calcified, but the calcium deposition did not appear to extend beyond the margin of the flap (Figure 1). It was impossible to determine the depth of involvement. The fundus examination revealed a hole in the temporal macula, but the dense band keratopathy limited the view of the posterior pole (Figure 2).
HOW WOULD YOU PROCEED?
1. Would you debride the calcific deposits from the cornea to allow for retinal surgery with a view through a debrided surface?
2. Amputate the flap, since the calcific deposits clinically appear to be limited to the flap itself and not present in the stromal bed?
3. Place a temporary keratoprosthesis in order to allow retinal surgery to proceed and complete the case as a penetrating keratoplasty?
SURGICAL COURSE
Under normal circumstances, treatment options for band keratopathy depend on the symptomatology and the goal of removing the calcium. If the inciting stimulus for the development of band keratopathy is not eliminated, it is likely to recur.
One treatment option involves using disodium EDTA to chelate the plaque, in addition to mechanically debriding the calcific plaque. In this particular case, the risk of dislodging the LASIK flap or macerating the flap's edges—both of which would increase the risk of epithelial ingrowth—made this a poor choice. PTK is another technique that has been successful in the treatment of limited band keratopathy.1 The procedure's efficacy may be related to the complete removal of Bowman's layer during the ablation, which eliminates the scaffolding for the calcific deposits. The deposits in this case, however, were far too extensive to remove with PTK.
The definitive treatment for band keratopathy is penetrating keratoplasty, but there is an increased incidence of graft failure when a penetrating keratoplasty is performed in the presence of silicone oil. In one series of 14 corneal transplantation patients, the frequency of graft failure was 25% when silicone oil was removed at the time of penetrating keratoplasty, and 67% when silicone oil was retained in the eye. The mean graft survival rate in this group of patients was 25 months, ranging from 2 to 61 months. Studies show that, if silicone oil remains in contact with a corneal transplant, then the corneal transplant will fail as a result of contact with the oil.2
The patient underwent surgery. We easily lifted the flap and noted that the calcium was limited to the flap itself. We observed no calcific deposits in the underlying stromal bed. The view to the posterior pole was still inadequate for the retinal surgeon to proceed, so we chose to amputate the flap, perform a trephination of the underlying cornea, and place a temporary keratoprosthesis in order to allow visualization during an additional vitrectomy and removal of the silicone oil. We then replaced the keratoprosthesis with a donor cornea to complete the penetrating keratoplasty procedure (Figure 3).
When selecting a surgical intervention, we considered the risk of graft failure associated with keeping the silicone oil and the risk of retinal redetachment associated with the removal of silicone. Due to the severity and recurrence of the retinal detachment, we performed the penetrating keratoplasty with the continued presence of silicone oil and planned to remove it in the future.
OUTCOME
The band keratopathy did not recur during the 1-year follow-up, and the patient's BCVA was 20/300 with a refraction of +5.00 +3.00 X 135. One year postoperatively, the graft was clear, with diffuse guttata and a central pachymetry measurement of 694 µm. Posterior segment abnormalities contributed to the limited BCVA.
DISCUSSION
Calcific deposits in the cornea can be associated with systemic causes such as hypervitaminosis D, hyperparathyroidism, sarcoidosis, and metabolic alkalosis. Topical agents, including sulfacetamide and drops containing the preservative phenylmercuric nitrate (as in pilocarpine), are also associated with band keratopathy.3 Additionally, the condition can occur with ocular changes (such as severe dry eye and uveitis) and in the presence of silicone oil. Band keratopathy can also be seen in phakic eyes with no silicone oil in the anterior chamber.
Pathologically, band keratopathy occurs due to a deposition of calcium carbonate in the interpalpebral basal epithelium, superficial stroma, and Bowman's layer.4,5 The reason for the preferential deposition of calcium within the interpalpebral area is unclear, but it may result from an elevation of pH in this area owing to tear evaporation.6 In a typical patient with band keratopathy, there is a lucid interval between the band and the limbus due to the buffering capacity of the limbal blood supply not available centrally in the cornea.7 In this patient, Bowman's layer was incised during the microkeratome pass in the LASIK procedure 1 year prior to the onset of the band keratopathy. This incision of Bowman's layer defined the limits of the calcium deposition and may help us to further understand the pathophysiology of this condition. This incision may have led to local changes in pH or neurotrophic changes that increased the possibility of calcific deposition in the LASIK flap but not the remaining cornea.
Laura T. Muller, MD, is the CIBA Vision/Novartis Ophthalmics Cornea Fellow at Rush-Presbyterian-St. Luke's Medical Center in Chicago. She may be reached at (847) 432-6010; lauramuller@hotmail.com.
Kirk H. Packo, MD, is Associate Professor of Ophthalmology at Rush-Presbyterian-St. Luke's Medical Center in Chicago. He may be reached at (312) 942-2117; khpacko@mindspring.com.
Holly M. Spanggord, MD, is a corneal specialist in private practice in Laguna Beach, California. She may be reached at (949) 558-2020; hspanggord@yahoo.com.
Randy J. Epstein, MD, is Associate Professor of Ophthalmology at Rush-Presbyterian-St. Luke's Medical Center in Chicago. He may be reached at (847) 432-6010; repstein@chicagocornea.com.
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