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Corneal graft failure due to migration of Ozurdex™ implant into the anterior chamber.

ABSTRACT: Purpose:We report a case of corneal endothelial graft failure secondary to dexamethasone intravitreal implant (Ozurdex™) migration into the anterior chamber (AC). Observations:A 53-year-old man with a history of bilateral idiopathic chronic uveitis, had a right anterior vitrectomy and AC intraocular lens (ACIOL) with a peripheral iridotomy. He received an intravitreal Ozurdex™ implant for right cystoid macular oedema (CMO). Three months later he developed pseudophakic bullous keratopathy and underwent a Descemet stripping automated endothelial keratoplasty (DSAEK), combined with IOL exchange (ACIOL explantation followed by scleral fixated posterior chamber IOL). He developed recurrent CMO post-operatively, for which he had a second Ozurdex™ implant. Six weeks following the implant he presented with reduced vision and corneal graft failure with migration of the Ozurdex™ implant into the AC. Despite prompt surgical removal of the implant, the graft did not recover and he underwent a repeat DSAEK. Conclusions and importance:Ophthalmologists should be aware of this adverse event and the importance of early implant removal to reduce the risk of permanent corneal oedema.

SUBMITTER: Madi HA

PROVIDER: S-EPMC5731668 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Corneal graft failure due to migration of Ozurdex™ implant into the anterior chamber.

Madi Haifa A HA Morgan Stephen J SJ Ghosh Saurabh S

American journal of ophthalmology case reports 20170901

<h4>Purpose</h4>We report a case of corneal endothelial graft failure secondary to dexamethasone intravitreal implant (Ozurdex™) migration into the anterior chamber (AC).<h4>Observations</h4>A 53-year-old man with a history of bilateral idiopathic chronic uveitis, had a right anterior vitrectomy and AC intraocular lens (ACIOL) with a peripheral iridotomy. He received an intravitreal Ozurdex™ implant for right cystoid macular oedema (CMO). Three months later he developed pseudophakic bullous kera ...[more]

PMID: 29260111

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Project description:The reduced hardware design of narrow implants increases the risk of fracture not only of the implant itself but also of the prosthetic constituents. Hence, the current study is aimed at estimating the probability of survival of anterior crowns supported by different narrow implant systems. Three different narrow implant systems of internal conical connections were evaluated (Ø3.5 × 10?mm): (i) Active (Nobel Biocare), (ii) Epikut (S.I.N. Implant System), and (iii) BLX (Straumann). Abutments were torqued to the implants, and standardized maxillary incisor crowns were cemented. The assemblies were subjected to step-stress accelerated life testing (SSALT) in water through load application of 30 degrees off-axis lingually at the incisal edge of the crowns using a flat tungsten carbide indenter until fracture or suspension. The use level probability Weibull curves and reliability for completion of a mission of 100,000 cycles at 80?N and 120?N were calculated and plotted. Weibull modulus and characteristic strength were also calculated and plotted. Fractured samples were analyzed in a stereomicroscope. The beta (?) values were 1.6 (0.9-3.1) and 1.4 (0.9-2.2) for BLX and Active implants, respectively, and 0.5 (0.3-0.8) for the Epikut implant, indicating that failures were mainly associated with fatigue damage accumulation in the formers, but more likely associated with material strength in the latter. All narrow implant systems showed high probability of survival (?95%, CI: 85-100%) at 80 and 120?N, without significant difference between them. Weibull modulus ranged from 6 to 14. The characteristic strength of Active, Epikut, and BLX was 271 (260-282)?N, 216 (205-228)?N, and 275 (264-285)?N, respectively. The failure mode predominantly involved abutment and/or abutment screw fracture, whereas no narrow implant was fractured. Therefore, all narrow implant systems exhibited a high probability of survival for anterior physiologic masticatory forces, and failures were restricted to abutment and abutment screw.

Project description:PurposeTo investigate the relationship between early post-operative anterior chamber inflammation (aqueous flare) and central corneal thickness (CCT) after cataract surgery and to evaluate the effect of anti-inflammatory prophylaxis on CCT.SettingDepartment of Ophthalmology, Rigshospitalet-Glostrup, University Hospital Copenhagen, Denmark.DesignPost-hoc analysis of a prospective randomized controlled trial.Patients and methodsA total of 470 participants who underwent standard cataract surgery were randomly allocated to prophylactic treatment with nonsteroidal anti-inflammatory drug (NSAID, groups C and D) or a combination of NSAID and steroid eye drops (groups A and B), commenced either pre-operatively (A and C) or post-operatively on the day of surgery (B and D), or "drop-less surgery" (peri-operative subtenon depot of dexamethasone, group E). Aqueous flare was measured before and three days after surgery. CCT was measured before surgery, three days, three weeks, and three months after surgery. Data were analyzed according to the intention-to-treat method.ResultsDoubling of aqueous flare increased mean CCT by 15.6 microns (95% CI 9.8; 21.3, P<0.001) three days after surgery. Mean CCT increased from 549 microns (95% CI 545; 552) at baseline to 594 microns (95% CI 585; 602) three days after surgery and returned to 551 microns (95% CI 545; 557) three months after surgery. Mean CCT was thinner in group C compared to group A three days after surgery. No difference was found for any other groups or time points.ConclusionIncreased anterior chamber inflammation was associated with significant corneal thickening three days after cataract surgery. Choice of anti-inflammatory regimen seemed to be of no or minimal importance on CCT when the effect of inflammation was accounted for. Corneal thickening is possibly mediated by underlying deterioration of the blood-aqueous barrier and corneal endothelium pump function caused by a post-operative inflammatory response.

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Corneal graft failure due to migration of Ozurdex™ implant into the anterior chamber.

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Corneal graft failure due to migration of Ozurdex™ implant into the anterior chamber.

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