Retinopathy of prematurity (ROP) is a vasoproliferative disorder of the retina and a leading cause of visual impairment and childhood blindness worldwide. The disease is characterized by an early stage of retinal microvascular degeneration, followed by neovascularization that can lead to subsequent retinal detachment and permanent visual loss. Several factors play a key role during the different pathological stages of the disease. Oxidative and nitrosative stress and inflammatory processes are important contributors to the early stage of ROP. Nitric oxide synthase and arginase play important roles in ischemia/reperfusion-induced neurovascular degeneration. Destructive neovascularization is driven by mediators of the hypoxia-inducible factor pathway, such as vascular endothelial growth factor and metabolic factors (succinate). The extracellular matrix is involved in hypoxia-induced retinal neovascularization. Vasorepulsive molecules (semaphorin 3A) intervene preventing the revascularization of the avascular zone. This review focuses on current concepts about signaling pathways and their mediators, involved in the pathogenesis of ROP, highlighting new potentially preventive and therapeutic modalities. A better understanding of the intricate molecular mechanisms underlying the pathogenesis of ROP should allow the development of more effective and targeted therapeutic agents to reduce aberrant vasoproliferation and facilitate physiological retinal vascular development.

Cataract surgery is one of the most performed surgeries in the developed world. In addition to its significant impact on visual acuity, phacoemulsification has been hailed as a potential intraocular pressure (IOP)-lowering procedure. While current evidence suggests an overall significant and sustained decrease in IOP to exist after cataract surgery, the specific ocular characteristics that could help predict which patients are likely to benefit from this IOP-lowering effect remain unclear. This definition is important in glaucoma patients if this surgery is to be used in the treatment for this disease. Our review aims to summarize the literature on the subject, depicting possible mechanisms behind this IOP decrease, which type of patients are more likely to benefit from this surgery for IOP-lowering purposes and ultimately help optimizing disease management for the increasing number of patients with concomitant glaucoma and cataract.

Inflammation of renal interstitium and uveal tissue establishes the two components of tubulointerstitial nephritis and uveitis (TINU) syndrome. Although believed to occur more frequently in young females, a broad spectrum of patients can be affected. Both renal and eye disease can be asymptomatic and may not manifest simultaneously, having independent progressions. Renal disease manifests as acute kidney injury and may cause permanent renal impairment. Eye inflammation can manifest in different anatomical forms, most commonly as bilateral anterior uveitis and may progress to a chronic course. TINU syndrome accounts for approximately 1%–2% of uveitis in tertiary referral centres. A literature review covering the clinical features, pathogenesis, diagnosis and treatment is presented.

Purpose: Previous studies report that the response of retinal vessels to a decrease in oxygen (hypoxia) is vasodilation, thus increasing blood flow. We aimed to characterize the changes in retinal microvasculature induced by a mild hypoxia stress test in a healthy population, using ocular coherence tomography angiography (OCT‐A) technology.Methods: Interventional repeated‐measures study. The standardized hypoxia challenge test (HCT) was performed to all volunteers, according to the British Thoracic Society protocol. Ocular coherence tomography angiography (OCT‐A) was performed at three time‐points (baseline, during HCT and 30′ posthypoxia). Macular and peripapillary vessel densities were assessed using the built‐in software. To minimize bias, analysis was performed separately in right (OD) and left (OS) eyes. Repeated‐measures anova and mean comparison analysis were used as statistical tests (stata v13).Results: Studied population included 30 healthy subjects (14 women), with a mean age of 28.8 ± 4.2 [range 22–37] years. Baseline vessel density increased in hypoxic conditions and subsequently decreased to near‐baseline values in posthypoxia conditions. This pattern was observed for both eyes in both parafovea (OD: 55.3 ± 2.3 to 56.7 ± 1.9 to 55.8 ± 1.9, p < 0.05; OS: 56.9 ± 2.1 to 57.9 ± 1.9 to 57.3 ± 1.7, p < 0.05) and peripapillary (OD: 60.5 ± 0.5 to 62.6 ± 0.5 to 60.1 ± 0.4, p < 0.05; OS: 60.4 ± 0.4 to 62.3 ± 0.5 to 60.7 ± 0.4, p < 0.05) areas.Conclusion: To our knowledge, there are no published data specifically addressing mild hypoxia conditions and retinal microvasculature changes, using OCT‐A. This pilot study may pave way to better understand vascular responses in disease setting.

Purpose (1) To characterize the retrobulbar circulation in patients with optic disc drusen (ODD) using colour Doppler imaging; (2) to explore the differences in retrobulbar hemodynamics in patients with primary open‐angle glaucoma (POAG). Methods Retrospective analysis using three diagnostic groups: patients with ODD, age‐matched healthy controls and age‐ and visual defect‐matched patients with POAG. Subjects with history of ocular trauma or ocular diseases including vascular‐related diseases were excluded. Kruskal–Wallis and Spearman's correlation tests were performed to compare and explore the correlations between the hemodynamic parameters and visual field damage. Results Sixty patients were included and equally divided between the three groups. Patients with ODD had lower systolic and diastolic flow velocities in the central retinal artery (CRA) when compared to healthy individuals, but no difference was found with the glaucoma group (p < 0.005 versus healthy; p range 0.30–0.37 versus POAG). The systolic shift in flow patterns correlated with the extent of visual field defect in ODD patients (p < 0.001, r = −0.78, confidence interval: −0.43 to −0.92), but not in POAG (p = 0.73). Short ciliary arteries from ODD patients had lower mean systolic flow velocities when compared to both healthy individuals and patients with POAG (p < 0.01 versus healthy; p ≤ 0.04 versus POAG). The ophthalmic artery in ODD group had significantly higher mean blood velocities than in the POAG (p = 0.04), while showing a significant overlap in Doppler waveform variables to the control group (p range 0.08–0.97). Conclusions Similar to patients with glaucoma, individuals with ODD have low blood flow velocities in the vessels around the optic nerve head. Unlike patients with glaucoma, however, their CRA's blood flow velocity patterns correlate with the extent of the visual field defects.

Purpose: We hypothesize that patients with type 1 diabetes (T1D) may have abnormal retinal vascular responses before diabetic retinopathy (DR) is clinically evident. Optical coherence tomography angiography (OCTA) was used to dynamically assess the retinal microvasculature of diabetic patients with no clinically visible retinopathy. Methods: Controlled nonrandomized interventional study. The studied population included 48 eyes of 24 T1D patients and 24 demographically similar healthy volunteers. A commercial OCTA device (AngioVue) was used, and two tests were applied: (1) the hypoxia challenge test (HCT) and (2) the handgrip test to induce a vasodilatory or vasoconstrictive response, respectively. The HCT is a standardized test that creates a mild hypoxic environment equivalent to a flight cabin. The handgrip test (i.e., isometric exercise) induces a sympathetic autonomic response. Changes in the parafoveal superficial and deep capillary plexuses in both tests were compared in each group. Systemic cardiovascular responses were also comparatively evaluated. Results: In the control cohort, the vessel density of the median parafoveal superficial and deep plexuses increased during hypoxia (F_1,23 = 15.69, P < 0.001 and F_1,23 = 16.26, P < 0.001, respectively). In the T1D group, this physiological response was not observed in either the superficial or the deep retinal plexuses. Isometric exercise elicited a significant decrease in vessel density in both superficial and deep plexuses in the control group (F_1,23 = 27.37, P < 0.0001 and F_1,23 = 27.90, P < 0.0001, respectively). In the T1D group, this response was noted only in the deep plexus (F_1,23 = 11.04, P < 0.01). Conclusions: Our work suggests there is an early impairment of the physiological retinal vascular response in patients with T1D without clinical diabetic retinopathy.