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Editor,—Trabeculectomy combined with mitomycin C is becoming an acceptable alternative in the management of refractory glaucoma. We report on a patient who had received trabeculectomy with mitomycin C and demonstrated a large conjunctival bleb and well controlled intraocular pressure for 7 years but was lost follow up from 7–14 years postoperatively. Bilateral superior corneal ectasia was observed 15 years after the operation. The corneal ectasia may have been a coincidental episode or may have been induced by the bleb compression. However, we suppose that it was a late toxic complication of mitomycin C, which penetrated the corneal stroma during the operation and caused this episode.
A 49 year old man received the same operative procedures on both eyes as a result of open angle glaucoma in our clinic in March 1982. The procedure included a limbal based 3 × 5 mm partial thickness rectangular scleral flap centred on the 12 o’clock position and a 1 × 3 mm trapdoor combined with the intraoperative application of 0.2 mg/ml mitomycin C (MMC) soaking for 5 minutes. Before the operation, the best corrected vision was counting fingers 50 cm with –7.0 right eye and 20/100 with –6.0 –1.0 × 180 left eye. Intraocular pressure was 33 mm Hg right eye and 42 mm Hg left eye. Three months after the operation, the best corrected vision was 20/500 with –7.00 right eye and 20/200 with –3.50 left eye. During the 7 year follow up period, intraocular pressures of both eyes were well controlled around 6–12 mm Hg with prominent avascular blebs. He had been lost to follow up for 7–14 postoperative years. On a recent visit in March 1997, he complained of poor vision and saw the horizontal images much clearer than vertical images. Best corrected vision was 20/1000 with −3.25 −1.75 × 38 right eye and 20/200 with +1.75 −5.25 × 166 left eye. Slit lamp examination showed bilateral prominent cystic blebs at the superior limbal conjunctiva. The avascular blebs extended from 15 to 165 degrees, 3.7 mm wide in the right eye, and 45 to 150 degrees, 5.4 mm wide with a bleb invading across the limbus in the left. There was no evidence of a wound leak on Seidel test. Both optic discs were pale with the cup/disc ratio 0.9 right eye and 0.5 left eye. Corneal topography (Eyesys 2000) revealed bilateral ectasia at the superior corneas (Fig 1). The corneal thickness was measured by ultrasonic pachymetry at the corneal centre and 2.5 mm away from the centre in the direction of 45, 90, and 135 degrees. There were unremarkable changes in thickness around the ectatic sites on both corneas.
The mechanism of inducing such a late occurrence of superior corneal ectasia is not clear. It may merely have been a coincidental episode. The clinical findings are not similar to the degeneration, which frequently induces astigmatism, such as Terrien’s marginal degeneration, superior pellucid marginal degeneration,1senile marginal degeneration, or keratoconus. Several studies have reported the “with the rule” changes in corneal astigmatism in the early postoperative period of trabeculectomy.2 3 The changes that were usually under 2.5 dioptres and resolved within 12 weeks were not comparable with our findings. It is possible that a large cystic bleb, which is not uncommon after the trabeculectomy combined with MMC application, compressed the superior cornea, resulting in the changes of the corneal curvature and induced the ectasia. Another possibility is that this episode is directly related to the chronic toxicity of MMC that was applied 15 years ago. Taniharaet al reported prolonged impairment of peripheral corneal epithelial barrier function after the trabeculectomy.4 It verified the possibility that MMC can induce a late tissue dysfunction. In our case, MMC might have penetrated the stromal layer from the cutting edge of the scleral flap during the trabeculectomy causing keratocyte suppression, collagen degeneration, and finally corneal ectasia. The two postulated mechanisms mentioned above may act together. Further studies are necessary to prove this.
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