KPRO COMPLICATION

Sterile vitritis in eyes with Boston KPro type 1 karatoprostheses generally respond well to treatment. However, its recurrent form may result in more lasting damage, said Christina Marsica Grassi AB, MD, candidate at Harvard Medical School Massachusetts Eye and Ear Infirmary, Boston Massachusetts, US, at a Cornea Day session at the 18th ESCRS Winter Meeting in Ljubljana.
Ms Grassi presented a case report regarding a patient implanted with a Boston KPro type 1 keratoprosthesis who had three episodes of vitritis over the following eight years.
The patient was a 70-year-old male who was monocular from trachoma. He had undergone a KPro type 1 keratoprosthesis implantation after two prior failed corneal transplants. Some 13 months after undergoing implantation of the device he developed pain in his eye and his uncorrected vision decreased from 20/400 to light perception only.
Slit-lamp examination revealed trace cells in the anterior chamber and 1+ to -2 + cells in the vitreous. He had a well-placed keratoprosthesis. His B-scan confirmed vitreous debris but also showed the absence of retinal detachment.
He underwent a vitreous tap and received an injection of antibiotics and corticosteroids. He also received a sub-Tenons triamcinolone injection, and his topical steroids were increased. His cultures were negative and two-and-a-half weeks after the vitritis event, his visual acuity had returned to 20/400, although the vitreous took 11 weeks to clear.
Seven years later the same patient developed a second episode, this time with severe photophobia, tearing and a gradual drop in vision. His visual acuity dropped from 20/60 at last visit to 20/200. His IOP was 15 mmHg to 20 mmHg and he complained of having a tender eye.
Slit-lamp examination showed the presence of 2+ cells in the vitreous. The keratoprosthesis had no infiltrates. B-scan confirmed the presence of vitreous debris and showed no retinal detachment. Macular OCT confirmed that the fovea was normal.
The patient received an increase in his prednisolone, acyclovir and vancomycin and his moxifloxacin was stopped. He did not receive a triamcinolone injection. The vitreous took six days to clear. However, it took the patient nine weeks to achieve his best visual acuity of 20/100.
The patient’s third vitritis episode occurred one-and-a-half years later. This time, he presented with an acute overnight loss of vision, but without pain or any discharge. His vision was limited to light perception. Slit lamp confirmed 3+ cells in the vitreous and a quiet anterior chamber. This time his B-scan showed significant macular thickening.
The patient’s condition did not respond to a sub-Tenons injection of triamcinolone or intravitreal antibiotics. Three days later the patient underwent pars plana vitrectomy. At two weeks follow-up macular OCT revealed loss of inner segment/outer segment contours and vitreomacular traction on the fovea.
The reasons for the recurrences and for the failure of therapy are not clear, but a microscopic break in the seal at the juncture of the artificial cornea and its carrier graft tissue optic may have played a role, Ms Grassi said.
Christina Marsica Grassi: mary_leach@meei.harvard.edu
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