A female toddler clinically diagnosed with hand, foot and mouth disease (HFMD) was referred by the treating paediatrician, with acute-onset painless diminution of vision for 3 days. She had papulomacular skin rashes and was unable to follow the light stimulus at presentation. On fundus evaluation, bilateral asymmetrical (left eye more severe than the right eye) multifocal full-thickness necrotising retinitis, occlusive haemorrhagic retinal vasculitis, optic disc pallor and left eye exudative retinal detachment (eRD) were noted. Due to the background of HFMD and unexpected prompt response of intravitreal and systemic corticosteroids, a preliminary diagnosis of bilateral presumed enterovirus-associated retinopathy was established. The patient showed a favourable response to a weekly taper of oral steroids for the next 3 months. The retinitis, vasculitis and eRD were resolved with widespread retinal pigment epithelium (RPE) atrophy.HFMD with retinopathy secondary to presumed enterovirus infection, though rare, can present with extensive RPE and optic disc atrophy despite administration of oral corticosteroids.

Photoreceptor (PR) loss causes vision loss in many blinding diseases and effective therapies to prevent this cell loss are lacking. Aspartate aminotransferases (GOTs), located in the cytosol (GOT1) and mitochondria (GOT2), are key components of the malate-aspartate shuttle, which transfers reducing equivalents from cytosol to mitochondria. Previous work has implicated the GOTs as potential modulators of blinding retinal disease. To determine the roles of GOT1 and GOT2 in rod PRs, we generated rod PR-specific Got1 or Got2 conditional knockout mice (Got1 or Got2 cKO). We previously showed that Got1 cKO causes PR degeneration and is accompanied by NADH accumulation and a decreased retinal NAD+/NADH ratio. Here, we show that NADH oxidation via metabolic or genetic means prolongs PR survival in Got1 cKO animals, implicating NADH accumulation, or reductive stress, as a key driver of PR degeneration. In contrast, Got2 cKO causes minimal PR degeneration and alterations in retinal NADH and the NAD+/NADH ratio that oppose reductive stress. Interestingly, GOT2, but not GOT1, is decreased in multiple models of PR degeneration, including retinal detachment (RD) where the NAD+/NADH ratio favors a reductive state. Notably, loss of Got2 in PRs demonstrates a neuroprotective effect after experimental RD suggesting decreased GOT2 expression may be part of a stress response to promote PR survival. Overall, this study illustrates the differential dependence on the GOTs for PR health, provides evidence that an overly reductive environment is detrimental to PR survival, and identifies GOT2 as a novel therapeutic target with potentially broad application in blinding diseases.

Proliferative diabetic retinopathy (PDR) is a leading cause of severe visual loss in working-age adults and represents the end stage of chronic neurovascular injury in diabetes. Despite advances in screening and treatment, including panretinal photocoagulation (PRP), intravitreal anti-vascular endothelial growth factor (anti-VEGF) agents and pars plana vitrectomy (PPV), outcomes remain heterogeneous: many eyes stabilise, whereas others progress to vitreous hemorrhage, tractional retinal detachment or neovascular glaucoma despite apparently adequate therapy. This review synthesises current knowledge on the pathophysiology, morphological phenotypes and treatment paradigms of PDR, with a specific focus on predictors of onset, progression, and recurrence. PDR is contextualised as a multifactorial neurovascular and inflammatory disease, integrating data on hypoxia-driven angiogenesis, glial activation, microvascular rarefaction, neurodegeneration, and vitreoretinal interface remodelling. Histopathological and multimodal imaging characteristics of neovascular complexes and the vitreoretinal interface are described, highlighting how phenotypes on colour fundus photography, widefield fluorescein angiography, optical coherence tomography (OCT), and OCT angiography relate to ischemic burden and clinical behaviour. Systemic, ocular, imaging, biomarker, and genetic factors associated with progression from non-proliferative diabetic retinopathy to PDR and with progression within established PDR after PRP, anti-VEGF therapy, and PPV are critically appraised. Across modalities, younger age, diabetes duration, poor glycaemic control, renal disease, extensive non-perfusion, high neovascular burden, complex fibrovascular proliferation, and incomplete or unsustained treatment consistently emerge as determinants of guarded outcomes. Outstanding gaps in mechanistic understanding, risk stratification, regenerative therapy, and implementation are identified, alongside a proposed research agenda aimed at delivering mechanistically grounded risk-prediction tools and disease-modifying interventions for PDR.

Topiramate-induced multifocal exudative retinal detachment is a rare but potentially vision-threatening adverse effect. We report a 59-year-old woman with idiopathic intracranial hypertension who developed painless bilateral blurry vision and color desaturation 8 days after initiation of topiramate 25 mg twice daily. Fundus examination and spectral-domain optical coherence tomography demonstrated bilateral multifocal exudative retinal detachment with subretinal fluid. Extensive infectious and inflammatory investigations were unremarkable. Topiramate was discontinued, resulting in complete anatomical resolution of subretinal fluid and improvement of visual acuity to 20/30 in both eyes over 3 months of follow-up. This case highlights the importance of recognizing this uncommon ocular complication and the potential for complete recovery following prompt drug cessation.

Sports-related ocular trauma is an important cause of preventable visual morbidity, particularly in contact sports such as football (soccer). Although many injuries initially present with mild anterior segment findings, significant posterior segment pathology may coexist and can be easily overlooked. We report the case of a 17-year-old male football player who presented with left eye pain, blurred vision, and periorbital bleeding following blunt ocular trauma during a football match. Examination revealed traumatic mydriasis with anterior uveitis, subconjunctival hemorrhage with conjunctival laceration and exposed Tenon's tissue, as well as commotio retinae with a peripheral horseshoe-shaped retinal tear. No retinal detachment was identified. The patient underwent prompt laser retinopexy and received topical anti-inflammatory and antibiotic therapy, resulting in favorable anatomical and visual outcomes. This case highlights the importance of maintaining a high index of suspicion in sports-related ocular trauma, as relatively subtle anterior segment findings may mask significant posterior segment injury. Careful and systematic anterior and posterior segment examination, including peripheral retinal evaluation, is essential to avoid missing sight-threatening complications and to ensure timely intervention.

High myopia is the leading cause of visual impairment worldwide, driven by excessive axial elongation resulting in biomechanical weakening of the sclera, and increasing the risk of complications such as posterior staphyloma, myopic macular degeneration, retinal detachment, cataract, and glaucoma. Conventional myopia management strategies aim to slow axial elongation in childhood, leaving patients with high myopia at risk of vision-threatening complications as they age. For these individuals, targeted therapies that strengthen the weakened sclera represent a promising, yet still experimental, approach. This review provides an overview of the role of the sclera in myopia progression, emphasizing changes in extracellular matrix composition, collagen organization, biomechanical integrity, and signaling pathways. Investigational scleral therapies are discussed, including posterior scleral reinforcement techniques, crosslinking modalities, pharmacological strategies, and tissue engineering approaches, with discussion of their mechanisms, preclinical and clinical evidence, and translational challenges. Particular attention is given to translational barriers, such as safe delivery to the posterior pole, retinal safety, and the absence of standardized outcome measures that link biomechanical reinforcement to functional benefit. Advances in imaging and in vivo biomechanical assessment, such as polarization-sensitive optical coherence tomography, Brillouin microscopy, and ultrasound-based elastography, hold promise for earlier risk stratification and treatment monitoring. By integrating insights from biomechanics, molecular biology, and therapeutic innovation, this review highlights the sclera as both a key driver of myopia pathology and a promising therapeutic target. Continued interdisciplinary collaboration will be essential to translate these experimental approaches into clinically viable treatments capable of reducing the growing burden of high myopia worldwide.

Serous retinal detachment (SRD) is an uncommon but vision-threatening manifestation of hypertensive disorders of pregnancy, particularly in the context of severe preeclampsia and hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. We report two cases of young primigravid women who developed bilateral SRD associated with HELLP syndrome. Both patients presented with acute bilateral vision loss and were diagnosed using optical coherence tomography. Management included antihypertensive therapy, magnesium sulfate, and delivery without any ophthalmological intervention. Both patients experienced complete visual recovery within two weeks. This report underscores the importance of prompt recognition, appropriate obstetric management, and the typically favorable visual prognosis of SRD in preeclampsia.

Retinal vasoproliferative tumors (RVPTs) are rare, benign lesions appearing as elevated, pink masses in the peripheral retina. Initially considered acquired retinal capillary hemangioblastomas, RVPTs are now recognized as distinct entities, with idiopathic and secondary forms. Though primarily affecting individuals between 30 and 50 years of age, their pathogenesis remains under investigation.