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Apparent Sudden Visual Loss: An Essential Approach
Published in Amy-lee Shirodkar, Gwyn Samuel Williams, Bushra Thajudeen, Practical Emergency Ophthalmology Handbook, 2019
Retinal vein occlusion: Management depends on a range of factors including whether it is central, branch or hemiretinal, ischaemic or non-ischaemic, presence or absence of neovascularisation, anterior chamber angle open or closed, IOP, VA and features on FFA. Treatments for macular oedema include anti-vascular endothelial growth factor (VEGF) therapy, dexamethasone implant (Ozurdex® from Allergan) and laser. The Royal College of Ophthalmologists has produced guidelines on the management of retinal vein occlusions considering all these specific factors. Neovascular age-related macular degeneration is usually managed by a dedicated macular service with anti-VEGF therapies including ranibizumb (Lucentis® from Novaritis) and aflibercept (Eylea® from Bayer). Ultimately, refer patients to your MR service for definitive management, remembering that neovascular complications should either be seen by them within 2 weeks and if this is not guaranteed consider performing pan retinal photocoagulation in clinic.
Swarm Intelligence and Evolutionary Algorithms for Diabetic Retinopathy Detection
Published in Sandeep Kumar, Anand Nayyar, Anand Paul, Swarm Intelligence and Evolutionary Algorithms in Healthcare and Drug Development, 2019
Sachin Bhandari, Radhakrishna Rambola, Rajani Kumari
Any edema hard exudate or ischemia which involves the fovea is termed diabetic maculopathy, and this is the most common cause of vision impairment in diabetes, especially those with type 2 diabetes as there are few different types of Maculopathy is their focal in one area diffuse spread all around ischemic or clinically significant macular edema[1]. Here we discuss clinically significant macular edema because it is the clinically significant. It is observed in an image of a blurry macula with some dot haemorrhages with hard exudates near, hence a thickened macula is actually easier to detect on OCT.
The Posurdex biodegradable intravitreal extended-release implant
Published in A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha, Vitreoretinal Surgical Techniques, 2019
Kulkarni Amol, Kuppermann Baruch D, Thomas Edgar L
Macular edema is a common cause of visual loss caused by a variety of possible insults to the retina. The various pathophysiologic mechanisms responsible for macular edema are intraocular inflammation, vitreoretinal traction, and vascular incompetence (diabetes and retinal vein occlusion disorders).1 Treatments targeting the particular pathophysio-logical mechanism may cause resolution of macular edema in most cases. The therapeutic modalities currently available for macular edema include medical treatment with topical and/or systemic nonsteroidal anti-inflammatory agents, corticosteroids, and acetazolamide, laser photocoagulation, and surgery to relieve traction.1 The management challenge, however, arises in cases with chronic and persistent macular edema. Potent corticosteroids such as triamcinolone acetonide, fluocinolone acetonide and dexamethasone can be very effective in these cases, but the clinician must be alert to the potential toxic effects after prolonged systemic administration.2 Site-specific delivery of the drug in the vitreous cavity may be able to achieve a high concentration and eliminate these systemic side-effects.
Triamcinolone acetonide injectable suspension for suprachoroidal use in the treatment of macular edema associated with uveitis
Published in Expert Review of Ophthalmology, 2022
Joanne Thomas, Lucas Kim, Thomas Albini, Steven Yeh
Uveitis, inflammation of the uveal tract, which includes the iris, ciliary body, and choroid, can be divided into infectious and noninfectious etiologies. In the developed world, noninfectious uveitis comprises 90% of all cases of uveitis and accounts for 10–15% of blindness [1,2]. About one-third of the cases of blindness in the developed world are due to uveitis-associated macular edema (UME) with a higher prevalence of macular edema in cases of intermediate uveitis and panuveitis [3]. Macular edema is caused by the breakdown of the blood-retinal barrier and may lead to thickening of the retina due to extracellular fluid [4]. Treatment in patients with noninfectious uveitis and secondary macular edema often consists of periocular corticosteroids for unilateral disease and systemic corticosteroids for bilateral disease as first line therapy [5]. Other treatments include corticosteroid-sparing immunosuppressive medication for patients who need long-term immunomodulation and local corticosteroid injections, particularly in individuals who wish to avoid systemic medications due to tolerability or side effect profiles.
Retinal vein occlusion: drug targets and therapeutic implications
Published in Expert Opinion on Therapeutic Targets, 2021
Alessandro Arrigo, Francesco Bandello
RVO is a leading cause of visual acuity loss in developed countries and affects patients with long life expectancy. The pathogenesis is extremely complex and involves both angiogenic and pro-inflammatory mediators. Current treatments include intravitreally administered anti-VEGF agents and corticosteroids. Both treatments have proved to be safe, well-tolerated and efficient in inducing macular edema reabsorption and visual acuity improvement. Anti-VEGF may be considered the option of choice on account of its extremely straightforward management, although these drugs are contraindicated for patients at high cardiovascular risk. Corticosteroids are highly efficient in reducing macular edema and inflammation but are strongly associated with intraocular pressure increases and cataract progression. The employment of prophylactic laser treatment is quite controversial and does not generally add significantly to the efficacy of intravitreal therapies. Current research is focused on the optimization of treatment strategies and on the development of treatments of longer duration, in order to reduce the burden of injections and to improve patient management. There is a considerable body of evidence revealing the involvement of many other mediators in the pathogenesis of RVO, and thus new potential therapeutic targets. From this point of view, the most intriguing prospect in the near future regards the development of new multitarget drugs, which might constitute further step forwards in the long-term management of RVO and improved outcomes for patients suffering from the condition.
Ischemia-Modified Albumin Levels and Thiol-Disulphide Homeostasis in Diabetic Macular Edema in Patients with Diabetes Mellitus Type 2
Published in Current Eye Research, 2021
Mustafa Kalayci, Ersan Cetinkaya, Kenan Yigit, Mehmet Cem Sabaner, Reşat Duman, Ahmet Rifat Balik, Özcan Erel
Diabetic retinopathy (DR) is a condition characterized by retinal angiopathy and neuropathy that occurs as a result of dysregulated blood glucose, and if left untreated, it may cause blindness.1 Diabetic retinopathy is the leading cause of untreatable vision losses in the population aged 20 to 65 years in developed countries.2 Long-term hyperglycemia-related toxicity is the primary mechanism in the development of DR. Long-term exposition to hyperglycemia is believed to result in a series of biochemical and physiological changes that ultimately lead to endothelial damage. Specific retinal capillary changes include capillary occlusion and thickening of basement membrane leading to retinal non-perfusion and decompensation of endothelial barrier function that results in pericyte losses and serum leakage, namely macular edema.3 The main cause of visual impairment in diabetic patients is diabetic macular edema. In general, macular edema is an indicator of fluid accumulation in the extracellular area in the retina in the macular region and threatens visual acuity if the retinal region in the macular center becomes thicker. Prevalence and severity of DR and macular edema show a positive correlation with abnormal hematological and biochemical parameters. However, the exact role of these abnormalities, either individually or in combination, in the pathogenesis of retinopathy has not been clearly defined yet.