Dorota Wyględowska-Promieńska

Neovascular age-related macular degeneration (nAMD) is a leading cause of irreversible central vision loss among older adults and is characterized by abnormal macular neovascularization, leading to exudation, hemorrhage, fibrosis, and progressive retinal damage. Advances in multimodal retinal imaging have substantially improved the diagnosis, classification, and management of nAMD. Optical coherence tomography (OCT) enables high-resolution cross-sectional visualization of retinal and choroidal microstructures, facilitating the detection of fluid accumulation, pigment epithelial detachments, fibrovascular tissue, and photoreceptor damage. OCT angiography (OCTA) complements structural imaging by enabling noninvasive visualization of the retinal and choroidal microvasculature and characterizing neovascular architecture without requiring dye injection. This chapter reviews the current clinical spectrum of exudative AMD based on OCT and OCTA findings, including type 1, type 2, type 3, mixed macular neovascularization, and polypoidal choroidal vasculopathy. Characteristic structural and vascular imaging biomarkers, including pigment epithelial detachment, intraretinal and subretinal fluid, prechoroidal clefts, the onion sign, branching vascular networks, vascular loops, and choriocapillaris alterations, are discussed along with their clinical significance and therapeutic implications. Representative OCT and OCTA images demonstrate the morphological diversity of individual lesion subtypes and highlight imaging features that are useful for diagnosis, assessment of disease activity, and monitoring of antivascular endothelial growth factor therapy. A comprehensive understanding of OCT- and OCTA-based biomarkers facilitates accurate differentiation of neovascular phenotypes, improves treatment monitoring, and supports individualized management of patients with nAMD.

Corneal diseases affect a significant proportion of the global population, with younger age groups being particularly vulnerable. In severe cases involving vision loss, standard techniques such as keratoplasty often fail. These cases require more invasive treatment through the implantation of artificial cornea or keratoprostheses. Since the development of the oldest technique for creating and implanting the first keratoprostheses by Strampelli, these devices have experienced major modifications to improve their biocompatibility, function, and long-term viability. As a result, there is currently a wide range of implants and procedures that are available and can be applied according to patient indications and clinical settings. This narrative review attempts to cover the literature on this topic by focusing on (1) recent advances in rigid (Boston Type I and II, osteo-odonto-keratoprosthesis, modified osteo-odonto-keratoprosthesis, and LV Prasad Eye Institute keratoprosthesis) and soft (AlphaCor, CorNeat, and EndoArt) keratoprosthesis designs and (2) more recent studies on innovative biomaterials and techniques that could lead to the fabrication of fully functional biosynthetic corneas with optimal properties. In our review of these materials, we cover the current clinical applications and limitations, as well as future prospects of less invasive and more efficient prostheses that could improve patient outcomes and quality of life.

Background: Post-traumatic corneal wounds that require suturing are quite common; they reduce corneal transparency and cause corneal distortion, leading to corneal astigmatism and higher-order aberrations. Excimer laser treatment can be a potentially beneficial intervention for such wounds. The observation aimed to evaluate the effectiveness of topography-guided custom ablation treatment (TCAT) in patients with corneal injuries. Methods: This observation included three patients with corneal penetrating trauma (full-thickness corneal scar) and one patient with corneal blunt trauma, i.e., a non-penetrating injury with corneal laceration (partial-thickness corneal scar). This cohort study was conducted from July 2021 to August 2023. After first-stage treatment (stabilization of the post-traumatic visual defect confirmed by refraction and topography examination, corneal healing, and improvement of the corneal scar), the patients underwent the second-stage treatment, i.e., TCAT with a 20 to 45 s application of mitomycin C solution to avoid haze induction. After TCAT, the uncorrected distance visual acuity (UDVA) and best-corrected distance visual acuity (BCVA) were measured. Refractive astigmatism was assessed using autorefractometry. Topographic astigmatism was analyzed using corneal topography and pachymetry. The root mean square (RMS) of the higher-order aberration was calculated using Zernike coefficients. The patients’ corneal healing and refractive changes were monitored. Results: All patients were monitored for corneal healing and refractive changes and underwent the same second-stage treatment, which utilized TCAT to regularize the corneal surface and reduce higher-order aberrations (HOAs). The UDVA of patients 1, 2, 3 and 4 improved by 3, 7.5, 4 and 6 rows (Snellen chart), respectively. The resultant UDVA was 1.0, 0.9, 0.7 and 1.2, while BCVA was 1.0, 1.2, 1.0, and 1.5, respectively. Conclusions: TCAT regularized the patients’ corneal surfaces and reduced HOAs. We, therefore, conclude that TCAT may be a beneficial second-stage treatment for corneal trauma-induced astigmatism.

Our study aimed to assess the anatomical changes in the retina, including the assessment of the reduction of diabetic macular edema (DME) on optical coherence tomography (OCT) and the improvement of retinal microvascular parameters, defined by the reduction of nonperfusion areas on OCT angiography (OCTA) after intravitreal injections of 6 mg faricimab, an anti-VEGF drug used in the treatment of DME. The study included twenty-two patients aged between 61 and 74 years, each of whom received four loading doses of 6 mg faricimab at 1-month intervals, as described in the summary of product characteristics. Hemodynamic parameters were analyzed by OCT angiography before the first intravitreal injection of faricimab and one month after each subsequent injection. The following parameters were analyzed: non-perfusion area (NPA), superficial capillary plexus (SCP) and deep capillary plexus (DCP), outer retinal flow area (ORFA), choriocapillaris flow area (CCFA) and foveal avascular zone (FAZ). Despite differences in the magnitude of improvement and time to improvement from the start of treatment with intravitreal injections of 6 mg faricimab, reductions in DME and improvements in OCTA parameters resulted in increased retinal blood flow and better visual acuity.

Age-related macular degeneration (AMD) is the leading cause of irreversible blindness worldwide and a severe medical and social problem. The steadily increasing number of patients is related to the aging of the population. So far, many factors affecting the development of AMD have been identified, which can be divided into non-modifiable, including genetic factors, age, and sex, and modifiable or environmental factors, such as smoking, poor diet, and hypertension. Early stages of age-related macular degeneration are characterized by fundus drusen and abnormalities in the retinal pigment epithelium. In late stages, geographic atrophy and choroidal neovascularization (CNV) are observed. The treatment of AMD, especially its advanced forms, is very challenging. Intensive research has made it possible to treat advanced stages of the dry form of AMD with pegcetacoplan and avacincaptad pegol, new drugs approved for use in the US. Pegcetacoplan targets the C3 and avacincaptad pegol targets the C5, the pivotal proteins of the complement cascade. The drugs are administered by intravitreal injection. The gold standard for neovascular AMD (nAMD) consists of intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) drugs such as bevacizumab, ranibizumab, aflibercept, brolucizumab, and faricimab. Treatment can be administered according to the fixed, pro-re-nata, and treat-and-extend regimens. The latter seems to have the best effect on improving visual acuity (VA) and the maximum therapeutic benefit. The search continues for the best ways to deliver intravitreal drugs. Current methods include sustained-release implants and hydrogel platforms for drug release, while the most promising future pathways for treating dry and nAMD are stem cell and gene therapy.

Corneal neovascularization can impair vision and result in a poor quality of life. The pathogenesis involves a complex interplay of angiogenic factors, notably vascular endothelial growth factor (VEGF). This review provides a comprehensive overview of potential therapies for corneal neovascularization, covering tissue inhibitors of metalloproteinases (TIMPs), transforming growth factor beta (TGF-β) inhibitors, interleukin-1L receptor antagonist (IL-1 Ra), nitric oxide synthase (NOS) isoforms, galectin-3 inhibitors, retinal pigment epithelium-derived factor (PEDF), platelet-derived growth factor (PDGF) receptor inhibitors, and surgical treatments. Conventional treatments include anti-VEGF therapy and laser interventions, while emerging therapies such as immunosuppressive drugs (cyclosporine and rapamycin) have been explored. Losartan and decorin are potential antifibrotic agents that mitigate TGF-β-induced fibrosis. Ocular nanosystems are innovative drug-delivery platforms that facilitate the targeted release of therapeutic agents. Gene therapies, such as small interfering RNA and antisense oligonucleotides, are promising approaches for selectively inhibiting angiogenesis-related gene expression. Aganirsen is efficacious in reducing the corneal neovascularization area without significant adverse effects. These multifaceted approaches underscore the corneal neovascularization management complexity and highlight ideas for enhancing therapeutic outcomes. Furthermore, the importance of combination therapies and the need for further research to develop specific inhibitors while considering their therapeutic efficacy and potential adverse effects are discussed.

A healthy cornea is a nonvascularized, transparent tissue. It is nourished by diffusion through the tear film, aqueous fluid and neurotrophins supplied by the corneal innervation. The cornea is devoid of both blood and lymphatic vessels, which makes it an immunologi-cally privileged tissue. Corneal neovascularization develops due to an imbalance between angiogenic and anti-angiogenic factors and can lead to a significant decrease in visual acui-ty. It may cause scarring, lipid keratopathy, and corneal edema. The resulting pathological vascularization of the cornea reduces its immune privilege and significantly worsens the prognosis after subsequent penetrating keratoplasty, increasing the risk of rejection of the transplanted flap. Neovascularization is favored by many disease processes, including auto-immune diseases, viral inflammations, mainly herpes and varicella-zoster, and blepharitis [1]. There are several options to treat corneal neovascularization, both pharmacological and surgical. Angiostatic treatment involves inhibiting the growth of new vessels by suppressing inflammatory responses. VEGF inhibitors, steroids, cyclosporine A, and amniotic membrane grafts secured to the cornea work this way. VEGF inhibitors are the agents with the direct and most potent angiostatic effect. Angioregressive treatment, on the other hand, results in the regression of already existing pathological vessels. This therapy is also based on VEGF inhibitors, which, however, have the most potent effect on newly formed and small vessels but are less effective in reducing large-caliber and mature vessels. A more effective method for such vessels is ablation, which involves surgical closure. The most commonly used an-gio-occlusive method is needle diathermy and argon or yellow laser therapy. In advanced corneal neovascularization, corneal transplant surgery may be necessary. It is best performed after pretreatment with anti-VEGF preparations, often continued after corneal transplanta-tion to reduce the risk of transplant rejection [2]. This paper discusses the pathogenesis of corneal neovascularization and the current and future trends in its treatment.

Background: Cone–rod dystrophies (CRDs) are a heterogeneous group of inherited retinal diseases (IRDs) characterized by cone photoreceptor loss, that is followed by subsequent rod photoreceptor impairment. Case presentation: A 49-year-old man complaining of diminution of vision in both eyes (OU) was referred to our outpatient clinic. He reported visual loss for 5 years, but it was most progressive during the last few months. The best-corrected visual acuity (BCVA) at presentation was 0.4 in the right eye (RE) and 1.0 in the left eye (LE). Fundus fluorescein angiography (FFA) revealed granular hyperfluorescence in the macula and concomitant areas of capillary atrophy. Flash full-field electroretinography (ffERG) showed lowering of a and b waves as well as prolonged peak time in light-adapted conditions. However, outcomes of dark-adapted ERGs were within normal limits. Based on the constellation of clinical, angiographic, and electrophysiological tests findings, a diagnosis of IRD was suspected. Genetic testing showed a homozygous, pathogenic c.783G>A mutation in the cadherin-related family member 1 (CDHR1) gene, which confirmed CRD type 15 (CRD15). Conclusions: We demonstrate the clinical characteristics, retinal imaging outcomes, and genetic test results of a patient with CRD15. Our case contributes to expanding our knowledge of the clinical involvement of the pathogenic mutation c.783G>A in CDHR1 variants.

(1) Background: To compare the results of a new intraoperative contactless device (INTEGRA Optomed, Poland) with the result of a manual method for determining the axis for toric intraocular lens implantation. (2) Material and Methods: This retrospective observational study included 60 eyes of 40 patients (17 men, 23 women) who had toric intraocular lenses implanted. A video recording of each surgery that used the INTEGRA system was made for the analysis. Two researchers then independently assessed the location of the implant axes determined with both digital and manual slit-lamp methods, and compared the results between methods. (3) Results: The implantation axes suggested through the manual and INTEGRA methods were similar. The median axis disparities were 0.0 degrees for both groups. The standard deviation was 0.63 and 0.75 for researcher 1 and 2, respectively. The dominant value was 0.0 in both groups. The INTEGRA axis designation was statistically significantly different from the manual method for researcher 1 (p < 0.05), but it was statistically insignificant for researcher 2 (p = 0.79). (4) Conclusions: The INTEGRA system is a digital ink-free device for image tracking scleral vessels. It was helpful for determining the implantation axis in a precise manner, and the measurements were comparable with those obtained through a manual technique.

Background and Objectives: Topically administered antiglaucoma medications, especially those containing benzalkonium chloride (BAC), may cause local adverse effects and compromise ocular surface. The aim of the study was to assess the effect of topical prostaglandin F2α analogs (PGAs): preservative-free latanoprost, BAC-preserved latanoprost, preservative-free tafluprost, and BAC-preserved bimatoprost, on selected oxidative stress parameters in the tear film. Materials and Methods: The patients were divided into five groups: group C (n = 25) control group—subjects who did not use topical antiglaucoma medications, group L (n = 22)—patients using topical preservative-free latanoprost, group L+BAC (n = 25)—patients using topical BAC-preserved latanoprost, group T (n = 19)—patients using topical preservative-free tafluprost, and group B+BAC (n = 17)—patients using topical BAC-preserved bimatoprost. The oxidative stress markers in the tear film samples were evaluated: total protein (TP) concentration, advanced oxidation protein products (AOPP) content, total sulfhydryl (-SH) groups content, the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as Total Oxidant Status (TOS), Total Antioxidant Response (TAR), and Oxidative Stress Index (OSI). Results: The TP concentrations in the groups L, L+BAC, and B+BAC were statistically significantly higher in comparison with group C. The SOD and CAT activities in the groups L+BAC and B+BAC were statistically significantly higher when compared to group C. As compared to group C, AOPP and TOS were statistically significantly higher in all the study groups. OSI was found to be statistically significantly higher in the groups L+BAC, T, and B+BAC in comparison with group C. Conclusion: Use of topical PGAs by the patients with ocular hypertension or primary open-angle glaucoma is associated with increased oxidative stress in the tear film which is additionally exacerbated by the presence of BAC in the formulation.