Purpose: To investigate the effect of serial anterior chamber (AC) paracenteses in eyes with sustained elevations of intraocular pressure (IOP) in the setting of repeated intravitreal injections (IVI) of anti–vascular endothelial growth factor medications. Methods: This is a retrospective records review of patients undergoing IVI of anti–vascular endothelial growth factor medication (bevacizumab, ranubizumab, or aflibercept), who demonstrated a sustained elevation of preinjection IOP and also received AC paracentesis immediately after IVI on at least three consecutive visits. Changes in preinjection IOP and cup-to-disk (C:D) ratio were compared before and after the initiation of IVI and before and after the introduction of AC paracenteses with each subsequent IVI. Results: Twenty-three eyes of 17 patients receiving a median of 26 IVI experienced a rise in preinjection IOP from 16.3 mmHg to 21.1 mmHg (P = 0.004) and an increase in mean C:D ratio from 0.37 to 0.47 (P = 0.0002). After introduction of AC paracenteses (median of 12), mean IOP was returned to baseline 16.00 mmHg (P = 0.002), mean C:D ratio stabilized (0.50, P = 0.197), and maximum IOP decreased from 26.8 mmHg to 23.0 mmHg (P = 0.05). Nineteen (82.6%) eyes required an increase in topical glaucoma medications during the study period, and 13 (56.5%) still required additional therapies after initiation of AC paracenteses. Five eyes (38.5%) required laser or glaucoma drainage device procedures. Conclusion: Serial AC paracenteses reduced immediate postinjection IOP, and along with standard glaucoma care in most patients, reversed preinjection IOP elevation, and stabilized optic nerve changes associated with repeated intravitreal anti–vascular endothelial growth factor injections in a subset of patients with sustained elevation of preinjection IOP.

PurposeTo report the only known case, to our knowledge, of bilateral exudative retinal detachments in the setting of thrombotic microangiopathy associated with intravenous abuse of extended-release oxymorphone (Opana ER).ObservationsA 35-year-old male presented with headaches and acute, painless vision loss in the context of daily IV abuse of crushed oral Opana ER. The patient was found to have microangiopathic hemolytic anemia (MAHA), acute kidney injury in conjunction with hypertensive crisis and bilateral exudative retinal detachments.Conclusions and importanceBilateral exudative retinal detachments are rare ophthalmic complications that have been reported with thrombotic thrombocytopenic purpura (TTP). Non-TTP thrombotic microangiopathy, initially described as a “TTP-like illness” consisting of MAHA and thrombocytopenia, has been associated with the IV abuse of Opana ER. We report a case of bilateral exudative retinal detachments due to thrombotic microangiopathy in the setting of IV abuse of Opana ER.

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Functions of Rx in Early Vertebrate Ocular Development Brian G. Zamora Patterning of the optic vesicle is a crucial step in early vertebrate eye development that organizes uncommitted optic vesicle cells into distinct distal, dorsal, and proximal regions that will give rise to the neural retina, retinal pigment epithelium (RPE), and optic stalk, respectively. Originating from the same sheet of anterior neuroectoderm, uncommitted optic vesicle cells are patterned into neural and non-neural (RPE) retinal domains through the coordinated activities of extrinsic signaling molecules and intrinsic transcription factors. Neural retinal specification is driven by FGF signals emanating from the surface ectoderm and developing lens, while RPE is specified by signals from the extraocular mesenchyme overlying the dorsal optic vesicle, likely a TGF-β superfamily protein. Similarly, signaling from the optic vesicle has been implicated in directing lens formation from cells in the surface ectoderm. Various experiments have shown that patterning of neural retina and RPE can be altered through the ectopic introduction of signaling molecules, or the manipulation of various developmentally regulated transcription factors. Indeed, in frogs, chicks, and rodents, determination of neural retina and RPE can be interchanged for some time after their initial specification: presumptive RPE cells can transdifferentiate into neural retinal cells, and vice versa, demonstrating the bipotentiality of optic vesicle cells. Specifically, numerous studies demonstrate FGFs, and downstream effectors of FGF signaling, are important mediators of RPE-to-neural retinal transdifferentiation. Rx is a paired-like homeobox gene that encodes a transcription factor that is expressed in retinal progenitor cells (RPCs) of the developing optic vesicle/cup. As the optic cup forms, Rx expression is restricted to the inner layer of developing optic cup (presumptive neural retina) and is terminated as retinal progenitors exit the cell cycle and differentiate into a neural retinal cell type. Rx expression is maintained through adulthood in Müller glial cells, which have been shown to function like neural retinal stem cells. During embryogenesis, mice homozygous for a targeted Rx-null allele fail to form optic vesicles, demonstrating Rx is intrinsically required for the earliest stage of eye formation-evagination of the optic vesicles. Given the expression of Rx in proliferating retinal progenitors, we hypothesize that following optic vesicle evagination, Rx plays a role in promoting the proliferation of retinal progenitors, which could impact retinal and lens morphogenesis, and is required for the specification and/or maintenance of neural retinal identity. In this dissertation, the functions of Rx during the early stages of vertebrate ocular development following optic vesicle evagination are ascertained through Rx loss-of-function studies using Cre/loxP conditional inactivation strategies. We demonstrate that inactivation of Rx during the optic vesicle stage, via the...

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