Article
Results of phototherapeutic keratectomy (PTK) in the treatment of recurrent corneal erosion syndrome (RCES) in dependence of ablation depth and genesis of erosion
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Published: | September 22, 2004 |
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Outline
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Objective
In the last years PTK has been established as a successful option in the treatment of RCES. This study investigates the relapse rate after PTK treatment in dependence of ablation depth and the genesis of RCES.
Methods
71 eyes with RCES underwent PTK with the Schwind Keratom F. 49 of 60 eyes with post-traumatic erosions were ablated with subepithelial technique and the other twelve transepithelially. Eyes with Map-Dot-Fingerprint-Dystrophy (n=10) were divided into 7 subepithelial and 3 transepithelial PTK treatments. The average ablation depth was 2.64 μm (1.9 to 5.0 μm). Perioperatively all patients got antibiotic eye drops. Ocular lubricating drops were applied for the postoperative long-term aftercare. Follow-up ranged from 2.97 to 7.11 years with a mean of 4.99 years.
Results
Five eyes (71.4%) with Map-Dot-Fingerprint-Dystrophy were free of relapse after subepithelial PTK and another 2 eyes (66.7%) after transepithelial PTK. There is no statistical significant difference concerning applied ablation depth and the erosion genesis in the dystrophy group. Eight eyes (66.7%) with post-traumatic erosions were free of RCES after transepithelial ablation. There is no statistical significant difference concerning applied ablation depth and the genesis of erosion genesis. Subepithelial PTK in eyes with posttraumatic RCES proved to be successful in 36 cases (73.5%). There is a significant correlation (p=0.033) between ablation depth and the genesis of erosion.
Conclusions
We recommend to do a deeper than applied ablation in the Map-Dot-Fingerprint group with RCES to induce the immunohistochemical effect closer to the basal lamina where the metabolic disorder supposed to be. In eyes with RCES of traumatic origin a superficial subepithelial ablation depth (2.5 to 3.0μm) proved to be successful (73.5%) due to local induction of a biochemical cascade at the subepithelial level of the dysmetabolism.