Endoscopy-assisted pars plana vitrectomy in retinal detachments associated with anterior proliferative vitreoretinopathy and epiciliary membranes.

BACKGROUND: Proliferative vitreoretinopathy (PVR) is the leading cause of recurrent retinal detachment. Anterior PVR can contribute to recurrent retinal detachment and is often difficult to remove during conventional pars plana vitrectomy. The purpose of this study is to report surgical outcomes of single endoscopy-assisted pars plana vitrectomy (E-PPV) in patients with tractional retinal detachments associated with anterior proliferative vitreoretinopathy and epiciliary membranes. METHODS: Retrospective review of E-PPV between 2017 and 2021 at a tertiary referral center. Inclusion criteria involved adult patients who underwent E-PPV for tractional retinal detachment with anterior PVR and epiciliary membranes. Data collection included patients' demographics, ophthalmic exam findings, and surgical outcomes. A series of independent sample tests of proportion were conducted using a p-value of 0.05 as the threshold for statistical significance. RESULTS: Eighteen out of 55 patients who underwent E-PPV met the inclusion criteria. There were six females (33%) and 12 males (p-value = 0.096). Age ranged between 27 and 82 years old (mean age 52.1 ± 17.3 years). Nine patients (50%) had a history of ipsilateral retinal detachment repair. Single E-PPV success rate was 100% after three months, and 94.4% at the latest follow up visit. Recurrent retinal detachment with posterior PVR occurred in one patient four months after surgery. Cataract progressed in 57% (8/14) of phakic patients, with 63% (5/8) undergoing cataract extraction surgery within the first postoperative year. CONCLUSION: E-PPV enabled epiciliary membrane and anterior PVR visualization and removal. The single E-PPV success rate remained high at the latest follow up visit. E-PPV enabled the preservation of the phakic lens in all study patients. Larger prospective studies are needed on the role of E-PPV in retina surgeries.

Bilateral Cystoid Macular Edema with Zanubrutinib Therapy: A Case Report.

We present a patient with recurrent mantle cell lymphoma (MCL) who was treated with zanubrutinib, a Bruton's tyrosine kinase inhibitor. He subsequently developed bilateral cystoid macular edema (CME) in both eyes. This is the first report of CME in a patient with MCL who was treated with zanubrutinib. CME was refractory to topical corticosteroid therapy, but sub-Tenon's steroid injections and holding off zanubrutinib managed to decrease the CME. Treatment managed to prevent further vision loss but did not restore lost vision. The prompt ophthalmic exam is recommended for patients on zanubrutinib with decreased vision.

Implementing Smartphone Tutorials for Patients With Severe Glaucoma.

Purpose The purpose of the study is to determine if instructional videos detailing the use of smartphone accessibility features may be used to improve quality of life and comfort with phone usage among patients with severe glaucoma. Design The design of the present study is an interventional case series. Methods The patients with vision loss due to severe glaucoma were recruited from one institution. Two surveys were completed to provide baseline data: one detailed their current use of smartphone accessibility features, and the other provided survey was the EuroQol 5 Dimension 5 Level (EQ-5D-5L) (EuroQol Group, Rotterdam, Netherlands), which is used to assess the quality of life. Then, the patients were shown a brief video with instructions on configuring the use of voice-over, magnification, and zoom functions, along with other features. To conclude, the patients completed the same surveys either at follow-up visits or by phone calls. Results Fifteen patients were recruited to participate in the study. At baseline, the participants used a median of one accessibility feature, with the most common feature being "text sizing/bolding." At follow-up, the participants averaged the gain of use of one accessibility feature and reported a decrease in text messaging visual limitation, although these findings did not reach statistical significance. Overall, the quality of life, as measured by the EQ-5D-5L, demonstrated a non-statistically significant increase of six points. Conclusions Despite the lack of statistical significance, our results indicate that providing instructional videos may benefit the patients' ability to navigate on their smartphones. Incorporating links or Quick Response (QR) codes to these instructional videos provides an opportunity to improve the quality of life at no additional risk to the patient. Further studies are needed with an increased population to investigate for any significance of our findings.

A Mouse Model of Schnyder Corneal Dystrophy with the N100S Point Mutation.

Schnyder corneal dystrophy (SCD) is a rare autosomal dominant disease in humans, characterized by abnormal deposition of cholesterol and phospholipids in cornea caused by mutations in the UbiA prenyltransferase domain containing 1 (UBIAD1) gene. In this study, we generated a mouse line carrying Ubiad1 N100S point mutation using the CRISPR/Cas9 technique to investigate the pathogenesis of SCD. In vivo confocal microscopy revealed hyper-reflective dot-like deposits in the anterior cornea in heterozygotes and homozygotes. No significant change was found in corneal epithelial barrier function or wound healing. Electron microscopy revealed abnormal mitochondrial morphology in corneal epithelial, stromal, and endothelial cells. Mitochondrial DNA copy number assay showed 1.27 ± 0.07 fold change in homozygotes versus 0.98 ± 0.05 variation in wild type mice (P < 0.05). Lipidomic analysis indicated abnormal metabolism of glycerophosphoglycerols, a lipid class found in mitochondria. Four (34:1, 34:2, 36:2, and 44:8) of the 11 glycerophosphoglycerols species identified by mass spectrometry showed a significant increase in homozygous corneas compared with heterozygous and wild-type mouse corneas. Unexpectedly, we did not find a difference in the corneal cholesterol level between different genotypes by filipin staining or lipidomic analysis. The Ubiad1N100S mouse provides a promising animal model of SCD revealing that mitochondrial dysfunction is a prominent component of the disease. The different phenotype in human and mouse may due to difference in cholesterol metabolism between species.