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Biochemical Markers in Ophthalmology
Published in Ching-Yu Cheng, Tien Yin Wong, Ophthalmic Epidemiology, 2022
Abdus Samad Ansari, Pirro G. Hysi
Non-exudative AMD remains a clinical challenge for clinicians to manage, given the difficulty in monitoring progression and lack of effective treatment. Proteomic studies have detected a moderate subclinical leakage of the blood–retinal barrier in this form of disease, suggesting that potentially harmful plasma components, including complement or iron, could enter the retina in AMD patients before advanced disease [161]. Therefore, therapies that stabilize the blood–retinal barrier might play a pivotal role in the future management of this disease.
Posterior relaxing retinotomy
Published in A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha, Vitreoretinal Surgical Techniques, 2019
Stephen A Meffert, Gholam A Peyman
Angiographic study supports the clinical impression that retinotomies cause no significant damage in the attached retina.25 Retinal perfusion is unaffected, and there is no breakdown of the blood–retinal barrier. Notably, angiography did not show evidence of significant fibrovascular reproliferation.
Chronic Hyperglycemia Impairs Vision, Hearing, and Sensory Function
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
The blood–retinal barrier is composed of both an inner and an outer barrier. The outer blood–retinal barrier refers to the barrier formed at the retinal pigment epithelial cell layer, and it functions, in part, to regulate the movement of solutes and nutrients from the choroid to the subretinal space. In contrast, the inner blood–retinal barrier, similar to the blood–brain barrier, is located in the inner retinal microvasculature and comprises the microvascular endothelium that lines these vessels.
Coats like response in healed choroiditis
Published in Ocular Immunology and Inflammation, 2022
Saurabh Verma, Indrish Bhatia, Mousumi Banerjee, Vinod Kumar
Abnormal telangiectatic retinal vessels accompanied with subretinal exudation with or without retinal detachment in association with other ocular or systemic disorder are included in Coats’-like response.1 The etiology of retinal telangiectasia, either congenital or secondary remains unclear till now. Tarkkanen et al.7 studied the histopathological specimen of retina in Coats’ disease and inferred functional or structural loss of the blood-retinal barrier with disorganization of mural architecture. Reese8 postulated that endothelial cell dysfunction causes localized microvascular atresia and occlusion, which leads to vascular ectasia and formation of collateral vessels. Thus, the possible etiology could be any vaso-occlusive event, autoimmune vasculopathy or chronic inflammation causing structural damage to retinal vasculature which may precede the development of retinal telangiectasias.6 The clinical significance of this entity arises from the fact that such an exudative response further deteriorates the visual acuity due to its involvement of the posterior pole. In our case, the damage to the retinal vasculature secondary to inflammatory response might have lead to the development of Coats’-like response. Early diagnosis of this response can halt the ongoing neovascular drive and stabilize the blood retinal barrier by treating with intravitreal anti-VEGFs/steroids and/or laser photocoagulation. It also reduces the need for vitrectomy in the future.
Retinal findings in glomerulonephritis
Published in Clinical and Experimental Optometry, 2022
Heather G Mack, Deborah J Colville, Phillip Harraka, Judith Anne Savige, Alessandro Invernizzi, Samantha Fraser-Bell
Whether complement dysfunction in retinal disease reflects local ocular complement abnormalities, abnormal complement formed in the liver and deposited in the eye, or a combination, is unclear. Large complement molecules are prevented from entering the retina by the blood-retina barriers. The inner blood-retina barrier consists of tight junctions between the non-fenestrated retinal capillary endothelial cells, surrounded by end-feet of Müller glial cells and astrocytes which secrete factors enhancing or disrupting the integrity of capillary endothelial cells. The outer blood-retina barrier is controlled by the RPE and is composed of tight junctions between the RPE cells. Bruch’s membrane, the semipermeable membrane between the RPE and the choriocapillaris, best thought of as a vessel wall between the RPE and choriocapillary basal laminae, provides a further barrier for the diffusion of molecules from the choroidal circulation into the retina.22
Clinical Features of Endogenous Endophthalmitis Secondary to Minimally Invasive Upper Urinary Tract Calculus Removal
Published in Ocular Immunology and Inflammation, 2022
Bingsheng Lou, Yi Sun, Jialiu Lin, Zhaohui Yuan, Liwen He, Chongde Long, Xiaofeng Lin
ESWL, URL and MPCNL are the minimally invasive procedures to manage urinary calculi. However, complications such as bacteriuria, bacteremia, urinary tract infection, urosepsis, endocarditis and EE still can occur.14,15 The plausible reasons for the EE complication are listed as follows. First, predisposing conditions are important in evaluating patients’ risk. Among the predisposing medical condition assessed in our study, diabetes mellitus, which was found in 7 patients (58%), was the most common condition associated with EE. A number of studies have reported similar findings.16–18 A possible explanation is the dysfunction of blood-retinal barrier permeability caused by diabetes, especially for those with poorly controlled glucose levels. Moreover, elevated urine glucose levels also contribute to the growth of microorganisms. Diabetes has also been reported to be an underlying disease in patients with urinary tract infection due to C. albicans,19 which may probably lead to EE. Second, before crushing stones, occult lower urinary tract latent infections may exist in some patients. Mechanical trauma to the ureter during urological procedures may also be encountered. The regressive ureteral catheter will transfer the microorganisms into the upper urinary tract, and the elevated pressure in the renal pelvis is likely to cause sepsis.10 Third, the double-J stent, which is indwelled postoperatively to drain urine and prevent ureterostenosis for 2 to 4 weeks, may be also a potential risk factor because the procedure and subsequent stent removal may damage urinary mucosa.