Boston keratoprosthesis type I in the elderly.

BACKGROUND/AIMS: To determine the outcomes of Boston type I keratoprosthesis implanted in elderly patients. METHODS: A retrospective case series was performed on patients at least 75 years old who received the Boston type I keratoprosthesis between 1 January 2007 and 31 December 2012. Preoperative diagnosis, interval visual acuity, keratoprosthesis retention and postoperative complications were recorded for each patient. RESULTS: Forty-four Boston type I keratoprostheses were implanted in 44 eyes of 43 patients. The most common indication for surgery was corneal graft failure (n=23; 52.3%) followed by corneal scar (n=8; 18.2%) and limbal stem cell dysfunction (n=8; 18.2%). All patients had preoperative visual acuity of ≤20/200. Thirty-six of 44 (82%) patients achieved visual acuity of 20/200 or better postoperatively, and 20 of those (55.6%) maintained 20/200 or better for 1 year after surgery. The median length of follow-up was 825 days (range: 27-2193 days), and at the last follow-up visit, 20 of 44 (45.5%) had 20/200 or better vision. The median best-corrected visual acuity (logMAR) improved from 2.6 preoperatively to 1.0 at 1 year postoperative (p<0.00001). Device retention at 1 year postoperative was 88.9%. The most common postoperative complications were retroprosthetic membrane formation in 20 patients (45.5%) and cystoid macular oedema in six patients (13.6%). One patient developed keratitis and consecutive endophthalmitis 2 months after surgery and required enucleation. CONCLUSIONS: Boston type I keratoprosthesis is an effective modality in corneal blindness in elderly patients. Failure to restore or maintain ambulatory vision was typically due to non-corneal comorbidities, often unrelated to the keratoprosthesis.

Periprosthetic Tissue Loss in Patients With Idiopathic Vitreous Inflammation After the Boston Keratoprosthesis.

PURPOSE: Idiopathic vitritis is a poorly understood complication after Boston keratoprosthesis surgery with unclear etiology. We sought to determine whether an association exists between periprosthetic corneal tissue loss and the development of idiopathic vitritis in keratoprosthesis recipients. METHODS: Thirteen Boston type I keratoprosthesis recipient eyes with a history of idiopathic vitritis and 34 type I keratoprosthesis recipient eyes with no history of idiopathic vitritis underwent anterior segment optical coherence tomography (AS-OCT) at a median time postoperatively of 2.4 years versus 1.9 years (range, 0.5-14.2 vs. 0.1-13.6 years), respectively. Areas of corneal graft tissue loss ("gaps") around the keratoprosthesis stem were identified and analyzed by 2 masked observers. The difference in the presence, number, and size of gaps was compared between cases and controls. RESULTS: A periprosthetic gap was identified more commonly in idiopathic vitritis cases than in controls on AS-OCT (11/13, 86% vs. 11/34, 33.3%, P < 0.001). The number of gaps between cases and controls was also significantly different (2.6 ± 1.6 vs. 0.5 ± 0.8, P < 0.001), but not the estimated gap area (0.056 ± 0.049 mm² vs. 0.039 ± 0.025 mm², P = 0.22). CONCLUSIONS: A significantly higher proportion of keratoprosthesis recipient eyes with idiopathic vitritis had corneal tissue loss around the keratoprosthesis stem than did controls. Tissue loss could serve as an entry point for debris or bacterial components, triggering idiopathic vitritis. Our study underscores the utility of AS-OCT imaging in the postoperative management of keratoprosthesis patients.

Idiopathic vitritis in the setting of Boston keratoprosthesis.

PURPOSE: The aim of this study was to revisit the clinical paradigm attributed to Boston keratoprosthesis recipients presenting with idiopathic vitreous inflammation. METHODS: A retrospective chart review was performed of keratoprosthesis recipients at Massachusetts Eye and Ear Infirmary, from January 2000 to August 2013, for demographic data, indication(s) for surgery, timing and presentation of vitreous inflammation, and best-corrected visual acuity at baseline, on presentation, and after resolution of vitritis. RESULTS: Twenty-three (23 eyes) of 346 patients developed idiopathic vitreous inflammation after keratoprosthesis implantation. Six of 23 patients presented with signs and symptoms similar to infectious endophthalmitis but were culture negative. The proportion of patients who fit the previous paradigm of sudden painless loss of vision without external signs of infection ("sterile vitritis") at their first presentation with vitritis was only 4 of 23. Vision decline was variable (median, 9 lines on Snellen chart; range, 0-24), as was time to recovery of best vision (median, 8.9 weeks; range, 0.9-36.7). Nine eyes had repeat bouts (43 episodes in 23 patients). Ten of 43 episodes did not recover to baseline vision. Seventeen of 23 eyes with idiopathic vitritis after keratoprosthesis later developed other complications. CONCLUSIONS: The current paradigm for idiopathic vitritis after keratoprosthesis implantation includes sudden painless loss of vision with full recovery of vision on treatment with periocular corticosteroids. However, idiopathic vitritis after keratoprosthesis can also mimic infectious endophthalmitis with pain and external signs of inflammation. Visual loss can be gradual. Vision may not recover to baseline despite treatment. Vitritis may be a part of a common pathway of chronic inflammation after keratoprosthesis.