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Purpose: A ranibizumab prefilled syringe (PFS) has been approved by the US Food and Drug Administration. Here we evaluate the use of the ranibizumab PFS for intravitreal injection by assessing whether the PFS enables healthcare providers to successfully prepare and administer an injection without prior training. Design: Simulated-use and actual-use human factors usability studies. Participants: Retina specialists and ophthalmic medical personnel. Methods: In a simulated-use summative usability study, retina specialists (n=15) and ophthalmic medical personnel (n=15) prepared the ranibizumab PFS and performed injections into a model eye. In an actual-use formative usability study (ClinicalTrials.gov identifier: NCT02698566), three assistants and three retina specialists prepared the PFS and performed intravitreal injections, respectively, in study eyes of patients with retinal diseases (n=35). Main Outcome Measures: Twelve tasks specific to the unpacking, preparing, and properly administering the PFS for intravitreal injection were evaluated by a study assessor. Task performances were evaluated for use errors, close calls, and operational difficulties. Post-injection subjective user evaluations were performed to assess ease of use. Results: All participants successfully performed all essential and safety-critical tasks without use error in both the simulated-use and actual-use human factors usability studies. The majority of participants rated the tasks required to use the ranibizumab PFS as "Easy" or "Very Easy." Conclusions: Both the simulated-use and actual-use usability studies yielded consistent data, showing that healthcare professionals are able to use the ranibizumab PFS by successfully performing all critical tasks involved in preparing and delivering an intravitreal injection. The simulated-use usability testing was sufficiently realistic and representative of real world use, and was appropriate and preferred over actual-use usability testing for proper evaluation of the product user interface.

Ocular histoplasmosis syndrome (OHS) is a chorioretinal disorder with a distinct fundus appearance that is commonly found in regions endemic for Histoplasma capsulatum. Choroidal neovascularization (CNV) secondary to OHS is considered one of the principal causes of central vision loss among young adults in endemic areas. Although there is no consensus regarding its pathogenesis, evidence points to Histoplasma capsulatum as the most probable etiology. Once considered an intractable hemorrhagic maculopathy, CNVs are now treatable. Extrafoveal CNVs are successfully treated with laser photocoagulation. Subfoveal and juxtafoveal CNVs are managed with anti-vascular endothelial growth factor therapy, photodynamic therapy, or a combination of both. Modern imaging technologies such as spectral-domain optical coherence tomography have improved our diagnostic abilities, making it easier to monitor disease activity and CNV regression. We review the epidemiology, pathogenesis, clinical manifestations, differential diagnosis, and current treatment of this disease.

To describe the structural characteristics of retinal angiomatous proliferation and chorioretinal anastomosis in childhood Coats disease and redefine the previously described macular fibrosis.Prospective observational case series of consecutive patients with Coats disease examined over a 1-year study period. Multimodal imaging, including color fundus photography, wide-field fluorescein angiography, and spectral domain optical coherence tomography, was used to identify the features of macular retinal angiomatous proliferation and chorioretinal anastomosis.Retinal angiomatous proliferation and chorioretinal anastomosis were present in 5 of 21 patients with Coats disease (24%). The lesions appeared as well demarcated, nodular retinal pigment epithelial detachments surrounded by exudate, with retinal vessels continuous with the underlying choroidal neovascularization.Retinal angiomatous proliferation and chorioretinal anastomoses are features observed in a number of children (24% in the present series) with Coats disease and macular involvement. This lesion represents a distinct macular variant of Coats disease that underlies at least a proportion (all in the present series) of the previously described "macular fibrosis" and "subretinal mounds."

This PVR summary was performed after analysing 30 PVR questionnaires from expert vitreoretinal surgeons. There are many tips and tricks shared by many of them despite they are referred to only one. I want to appreciate their kind collaboration with this chapter.

In a fresh RD surgery, what technique would you use to identify a retinal hole or microtear if you could not find it after looking for it?

BACKGROUND AND OBJECTIVE: To evaluate the association between temporal macular atrophy and the presence of neovascularization in eyes with sickle cell disease (SCD). PATIENTS AND METHODS: Retrospective, case-controlled study identifying 64 eyes from 38 consecutive patients with SCD. Dilated funduscopic examination and wide-field fluorescein angiography were used to identify the Goldberg stage of proliferative sickle cell retinopathy. Spectral-domain optical coherence tomography images were analyzed for the presence of temporal macular atrophy. The association between temporal macular atrophy and neovascularization was then evaluated. RESULTS: Temporal macular atrophy had a sensitivity of 27%, a specificity of 67%, a positive predictive value of 83%, and a negative predictive value of 13% for identifying neovascularization. CONCLUSION: Although the presence of temporal macular atrophy is not sensitive enough to be used as a screening test, if seen in a patient with SCD, the physician should be alerted to the strong possibility that peripheral neovascularization may be present. [ Ophthalmic Surg Lasers Imaging Retina . 2016;47:27–34.]

Background We investigated sera from elderly subjects with and without age-related macular degeneration (AMD) for presence of autoantibodies (AAbs) against human macular antigens and characterized their identity. Methods Sera were collected from participants in the Age-Related Maculopathy Ancillary (ARMA) Study, a cross-sectional investigation ancillary to the Health ABC Study, enriched with participants from the general population. The resulting sample (mean age: 79.2±3.9 years old) included subjects with early to advanced AMD (n = 131) and controls (n = 231). Sera were tested by Western blots for immunoreactive bands against human donor macular tissue homogenates. Immunoreactive bands were identified and graded, and odds ratios (OR) calculated. Based on these findings, sera were immunoprecipitated, and subjected to 2D gel electrophoresis (GE). Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to identify the targets recognized by circulating AAbs seen on 2D-GE, followed by ELISAs with recombinant proteins to confirm LC-MS/MS results, and quantify autoreactivities. Results In AMD, 11 immunoreactive bands were significantly more frequent and 13 were significantly stronger than in controls. Nine of the more frequent bands also showed stronger reactivity. OR estimates ranged between 4.06 and 1.93, and all clearly excluded the null value. Following immunoprecipitation, 2D-GE and LC-MS/MS, five of the possible autoreactivity targets were conclusively identified: two members of the heat shock protein 70 (HSP70) family, HSPA8 and HSPA9; another member of the HSP family, HSPB4, also known as alpha-crystallin A chain (CRYAA); Annexin A5 (ANXA5); and Protein S100-A9, also known as calgranulin B that, when complexed with S100A8, forms calprotectin. ELISA testing with recombinant proteins confirmed, on average, significantly higher reactivities against all targets in AMD samples compared to controls. Conclusions Consistent with other evidence supporting the role of inflammation and the immune system in AMD pathogenesis, AAbs were identified in AMD sera, including early-stage disease. Identified targets may be mechanistically linked to AMD pathogenesis because the identified proteins are implicated in autophagy, immunomodulation, and protection from oxidative stress and apoptosis. In particular, a role in autophagy activation is shared by all five autoantigens, raising the possibility that the detected AAbs may play a role in AMD via autophagy compromise and downstream activation of the inflammasome. Thus, we propose that the detected AAbs provide further insight into AMD pathogenesis and have the potential to contribute to disease biogenesis and progression.