Cell-Based Delivery Systems: Development of Encapsulated Cell Technology for Ophthalmic Applications
Glenn J. Jaffe, Paul Ashton, P. Andrew Pearson in Intraocular Drug Delivery, 2006
Retinal vascular proliferation can occur in a number of different sites within the eye, and plays a role in many ocular diseases. In age-related macular degeneration, angiogenesis of the choroidal vasculature can cause leakage of fluid and bleeding into the retina, subretinal, subretinal pigmented epithelium, and subneurosensory spaces, leading ultimately to loss of neural retinal elements. In diabetic retinopathy, neovascularization in the optic nerve and the retina leads to hemorrhaging within the vitreous cavity and subsequent retinal detachments from traction. In addition, angiogenesis within the iris (called rubeosis iridis) causes neovascular glaucoma. Delivery of antiangiogenic factors either alone or in combination with neurotrophic factors could significantly impact the progression of these diseases. Some antiangiogenic factors that are believed to be promising for the treatment of vasoproliferative diseases are inhibitors of vascular endothelial growth factor (VEGF), soluble receptors for VEGF, endostatin, angiostatin, and pigment epithelium-derived factor. These are all testable using existing well-established animal models that mimic these human diseases. Also see Chapter 5.
Diabetes and the Microcirculation
John H. Barker, Gary L. Anderson, Michael D. Menger in Clinically Applied Microcirculation Research, 2019
A proportion of IDDM patients (especially those with hypertension or poor glycemic control) go on to develop more marked background retinopathy, with the development of numerous blot hemorrhages; venous abnormalities, such as beading, reduplication, and looping; variations in arteriolar caliber and arteriolar obstruction leading to “sheathing”; and cotton wool spots, indicating areas of retinal ischemia, which are visible as areas of nonperfusion on fluorescein angiography. At this time, proliferation of microvessels within the substance of the retina leads to intraretinal microvascular abnormalities (IRMAs). Such changes, indicating severe retinal ischemia, are termed preproliferative and herald the development of neovascularization, with proliferation of fragile new capillaries in association with fibrous tissue, growing forward from the surface of the retina (proliferative retinopathy). The presence of these neovascular membranes in association with retraction of the vitreous leads to sight-threatening vitreous hemorrhage from the fragile new vessels. Subsequently, further traction on the retina can cause retinal detachment. Neovascularization of the iris (rubeosis iridis) may lead to the development of a painful and intractable form of glaucoma. IDDM patients become susceptible to the development of proliferative retinopathy after several years of diabetes, with a rapid increase in the incidence of this problem between 10 and 15 years, and thereafter a relatively constant incidence. Around 50% of IDDM patients are affected after 25 years of diabetes,43 and again, this is a less common problem in NIDDM, affecting around 20% of patients.45
Cryosurgery of the retina
A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha in Vitreoretinal Surgical Techniques, 2019
From July 1989 to June 1990, 27 diabetic eyes with a persistent vitreous hemorrhage were treated with pancryocoagulation.40 A vitreous hemorrhage suitable for cryopexy was one in which the blood did not settle inferiorly despite double patching and elevation of the patient’s head – maneuvers to enhance settling to make the retina visible for laser treatment. Preoperative visual acuity ranged between light perception and finger counting. In 17 of the 27 eyes, a rubeosis iridis grade II–IV was present.
Neutrophil-To-Lymphocyte Ratio as a Potential Biomarker of Neovascular Glaucoma
Published in Ocular Immunology and Inflammation, 2021
Aiping Zhang, Li Ning, Jianping Han, Yi Ma, Yingbo Ma, Wenjun Cao, Xinghuai Sun, Shengjie Li
Neovascular glaucoma (NVG) is a potentially blinding secondary glaucoma which resultes from tissue ischemia/hypoxia, and most commonly associated with diabetic retinopathy (DR) and retinal vascular occlusive diseases (RVO).1Twenty-two percent of Proliferative diabetic retinopathy (PDR) patients develop NVG, mostly bilaterally. Around 40–50% of patients with ischemic retinal venous occlusion will suffer from NVG and 80% of those cases occur within 6–8 months, and most frequently in the first 1.5–2 months.1–3 NVG can be divided into three stages according to its histological basis and clinical characteristics, including rubeosis iridis, NVG with open angle, and NVG with angle closure. Rubeosis iridis is the principal sign of ocular ischemia. If treated in a timely and appropriate manner at this stage, iris neovascular will regress and the neovascularization process will be halted without further visual function loss. Rubeosis iridis, a key stage in halting the development of NVG is often subtle and difficult for the clinician to diagnose at an early stage. It requires a high index of suspicion. There is also a lack of useful biomarkers.1Once the condition has advanced to the second or third stage, a dysfunction of angle drainage has occurred and becomes irreversible.2
Diagnosing retinal vasculitis and its implications for treatment
Published in Expert Review of Ophthalmology, 2019
Nesrine Abroug, Sourour Zina, Molka Khairallah, Imen Ksiaa, Melek Kechida, Hager Ben Amor, Sana Khochtali, Moncef Khairallah
Poor visual outcome in patients with RV may be related to macular complications including macular edema, serous retinal detachment, cystoid macular degeneration, macular atrophy, lamellar or full-thickness macular hole, epiretinal membrane, and macular ischemia. In 14–54% of eyes with idiopathic RV final visual acuity is worse than 20/40 [81]. Patients with occlusive RV have a significantly worse visual outcome than those with nonischemic RV. Neovascularization occurs in about 10–15% of patients with RV [81–84]. Infectious RV seems to have better visual outcome compared to noninfectious RV [85,86]. Subsequent inflammation-induced complications including recurrent vitreous hemorrhage, traction retinal detachment, rubeosis iridis, and neovascular glaucoma can lead to persistent visual loss.
Secondary enucleated retinoblastoma with MYCN amplification
Published in Ophthalmic Genetics, 2021
Alexandre P. Moulin, Christina Stathopoulos, Fabienne Marcelli, Jacqueline Schoumans Pouw, Maja Beck-Popovic, Francis L. Munier
Microscopically, the retina was diffusely infiltrated by a poorly differentiated retinoblastoma with extensive exophytic growth. The retinoblastoma cells contained enlarged angulated nuclei with occasional prominent nucleoli. Severe anaplasia was only focally observed. The retinoblastoma circumferentially extended from the superior ciliary body, with local invasion of the iris root and the angle, to the inferior equatorial choroid. The ciliochoroidal invasion measured 36 mm. Posteriorly, the tumor infiltrated the optic nerve, extending beyond the lamina cribosa (611 µm) with a total optic nerve involvement of 1.25 mm. Tumor cells also invaded the prehyaloid space, the vitreous, the posterior and anterior chambers. A superior scleral canal was also infiltrated, showing perineural invasion without extraocular spread. There was no Azzopardi phenomenon and no intratumoural endothelial cell proliferation. In the centre of the globe, partially preserved gliotic retina alternated with calcification foci and areas of necrosis. Anteriorly, there was rubeosis iridis with a closed angle.
Related Knowledge Centers
- Central Retinal Vein Occlusion
- Diabetes
- Diabetic Retinopathy
- Eye
- Ocular Ischemic Syndrome
- Retina
- Retinal Detachment
- Blood Vessel
- Iris
- Neovascularization