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Vivek A Koduri, Amit K Reddy, Jennifer L Patnaik, Alan G Palestine, Anne M Lynch, Mina B Pantcheva Department of Ophthalmology, University of Colorado School of Medicine, Aurora, CO, USACorrespondence: Mina B PantchevaDepartment of Ophthalmology, University of Colorado School of Medicine, 1675 Aurora Court, F731, Aurora, CO, 80045, USATel +1-720-848-2500Fax +1-720-848-4043Email mina.pantcheva@cuanschutz.eduPurpose: To evaluate if the addition of endoscopic cyclophotocoagulation (ECP) to uncomplicated phacoemulsification cataract extraction increases the risk of persistent anterior uveitis (PAU) compared to phacoemulsification alone.Patients and Methods: Retrospective analysis of patients who had either phacoemulsification alone or combined with endoscopic cyclophotocoagulation from January 1, 2014 to December 31, 2017. Visual acuity, intraocular pressure, presence of anterior chamber cells, and steroid usage were analyzed pre- and post-operatively. Patient eyes with a history of uveitis, autoimmune disease, complicated cataract surgery, combined surgery other than ECP, and less than 3 months of follow-up were excluded.Results: This study consisted of 4423 eyes from 2903 patients, meeting the inclusion criteria (phacoemulsification only group n=4242 and phacoemulsification/ECP group n=181 eyes). PAU developed in 14.9% in the phacoemulsification with ECP group compared to 1.7% who had phacoemulsification alone. White patients had a 17.9 (95% CI: 7.8– 41.1, p< 0.0001) increased odds of developing persistent anterior uveitis with a combined procedure compared to phacoemulsification only, while Non-white patients had a 5.8 (95% CI: 2.8– 12.1, p< 0.0001) increased odds. Despite the higher odds ratio in White patients, this group had a significantly lower rate of PAU compared to Non-white patients after phacoemulsification/ECP.Conclusion: The addition of endoscopic cyclophotocoagulation to phacoemulsification significantly increases the risk of developing PAU in the post-operative period compared to phacoemulsification alone.Keywords: minimally invasive glaucoma surgery, post-operative inflammation

A 50-year-old ophthalmic technician was referred by her retina specialist for urgent consultation due to markedly elevated intraocular pressure (IOP) unresponsive to medical therapy. Her history included chronic polyarticular juvenile rheumatoid arthritis and chronic uveitis requiring ongoing topical steroid therapy. She had a sub-Tenon injection of Kenalog (triamcinolone) 18 months prior to referral. Chronic topical anti-inflammatory therapy included nepafenac (Ilevro) and prednisolone acetate 2 times a day. Attempts to discontinue topical steroid resulted in worsening inflammation. The patient was referred when the IOP measured 44 mm Hg in the left eye despite aggressive medical therapy, including acetazolamide. The IOP improved slightly when loteprednol was substituted for prednisolone acetate. Current medications in the left eye include brimonidine 3 times a day, loteprednol 2 times a day, nepafenac 2 times a day, and fixed combination latanoprost + netarsudil at bedtime. Her only medication in the right eye was travoprost. She is intolerant to dorzolamide. She was also taking acetazolamide 500 mg 2 times a day. She was not taking any anticoagulants. Past surgical history included cataract surgery in each eye. She has not had laser trabeculoplasty in either eye. Examination revealed uncorrected visual acuity of J1+ in the right eye (near) and 20/30 in the left eye (mini-monovision). There was no afferent pupillary defect. There was mild band keratopathy in each eye while the central cornea was clear in both eyes without keratic precipitates. Here angles were open to gonioscopy without peripheral anterior synechia. There was mild to moderate flare in each eye with trace cells. The IOP was 17 mm Hg in the right eye and 31 mm Hg in the left. Central corneal thickness measured 560 μm and 559 μm in the right and left eye respectively. There was a well-positioned intraocular lens within each capsule with a patent posterior capsulotomy. There was mild vitreous syneresis but no vitreous cell. The cup to disc ratio was 0.5 in each eye with a symmetrical neural rim. The retina was flat without macular edema. Visual field was normal in both eyes (Figures 1 and 2). Optical coherence tomography of retinal nerve fiber layer (RNFL) is shown in Figure 3 and retinal ganglion cell layer is shown in Supplemental Figure 1 (http://links.lww.com/JRS/A756).JOURNAL/jcrs/04.03/02158034-202301000-00020/figure1/v/2022-12-26T045736Z/r/image-tiffJOURNAL/jcrs/04.03/02158034-202301000-00020/figure2/v/2022-12-26T045736Z/r/image-tiffJOURNAL/jcrs/04.03/02158034-202301000-00020/figure3/v/2022-12-26T045736Z/r/image-tiff Please comment on your management of this patient's left eye., (Copyright © 2023 Published by Wolters Kluwer on behalf of ASCRS and ESCRS.)

Purpose: Cataract surgery is a procedure by which the lens fiber cell mass is removed from its capsular bag and replaced with a synthetic intraocular lens. Postoperatively, remnant lens epithelial cells can undergo an aberrant wound healing response characterized by an epithelial-to-mesenchymal transition (EMT), leading to posterior capsular opacification (PCO). Aldose reductase (AR) inhibition has been shown to decrease EMT markers in cell culture models. In this study, we aim to demonstrate that AR inhibition can attenuate induction of EMT markers in an in vivo model of cataract surgery., Methods: A modified extracapsular lens extraction (ECLE) was performed on C57BL/6 wildtype, AR overexpression (AR-Tg), and AR knockout mice. Immunofluorescent staining for the myofibroblast marker α-smooth muscle actin (α-SMA), epithelial marker E-cadherin, and lens fiber cell markers αA-crystallin and Aquaporin 0 was used to characterize postoperative PCO. Quantitative reverse transcription PCR (qRT-PCR) was employed to quantify postoperative changes in α-SMA, vimentin, fibronectin, and E-cadherin. In a separate experiment, the AR inhibitor Sorbinil was applied postoperatively and qRT-PCR was used to assess changes in EMT markers., Results: Genetic AR knockout reduced ECLE-induced upregulation of α-SMA and downregulation of E-cadherin. These immunofluorescent changes were mirrored quantitatively in changes in mRNA levels. Similarly, Sorbinil blocked characteristic postoperative EMT changes in AR-Tg mice. Interestingly, genetic AR knockout did not prevent postoperative induction of the lens fiber cell markers αA-crystallin and Aquaporin 0., Conclusions: AR inhibition prevents the postoperative changes in EMT markers characteristic of PCO yet preserves the postoperative induction of lens fiber cell markers.

Purpose: To test for apoptotic photoreceptor cell death and caspase activation as a function of time after induction of an experimental retinal detachment., Methods: Retinal detachments were created in Brown Norway rats by injecting 10% hyaluronic acid into the subretinal space using a transvitreous approach. Light microscopy and terminal dUTP-biotin nick end-labeling (TUNEL) was performed at 1, 3, 5, and 7 days after detachment to assess for the morphologic features associated with apoptosis. Western blot analysis of retinal protein extracts was performed using antibodies against caspase-3, -7, and -9 and poly-ADP ribose-polymerase (PARP) at 1, 3, and 5 days after detachment., Results: Light microscopic analysis of detached retinas showed the presence of pyknotic nuclei in the outer nuclear layer and disruption of the normal organization of the photoreceptor outer segments. TUNEL-staining was positive in the outer nuclear layer only in the detached portions of the retina. Western blot analysis confirmed the time-dependent activation of caspase-3, -7, and -9 and PARP in the detached retinas. No morphologic stigmata of apoptosis or caspase activation was detected in attached retinas., Conclusions: The apoptotic photoreceptor cell death in experimental retinal detachments is associated with caspase activation.