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Disorders of Circulation of the Cerebrospinal Fluid
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Other causes of optic disc swelling or involvement of the optic disc should be considered: Optic disc drusen.Optic neuritis.Central retinal vein occlusion.Temporal arteritis.Ischemic optic neuropathy.
Ophthalmic Emergencies
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
Conditions to be considered include: Central retinal artery occlusion.Central retinal vein occlusion.Vitreous haemorrhage.Retinal detachment.Optic neuritis.
Thromboembolic Disorders Of The Eye
Published in Hau C. Kwaan, Meyer M. Samama, Clinical Thrombosis, 2019
These data are difficult to interpret for a number of reasons. Many authors did not report strict ophthalmoscopic and angiographic criteria for the diagnosis of complete central retinal vein occlusion. Some did not have a clear distinction between the complete and partial occlusion, nor between central and branch vein occlusion. The partial and the branch vein varieties have a much better prognosis and should be evaluated separately. The modality of anticoagulant therapy also varied. Furthermore, the patients did not have a significant period of therapy which was rigidly controlled by laboratory monitoring of the blood coagulation parameters. In spite of all of these drawbacks one can form the following general impressions. First, since the prognosis of the untreated cases was reported to be so poor, it is assumed that they belong to the variety of hemorrhagic retinopathy that Hayreh described.17–20 Second, the use of anticoagulants with or without the additional thrombolytic agents can improve the prognosis substantially.
Central Retinal Vein Occlusion Presumably Associated with Lupus Anticoagulant Induced by SARSCoV-2
Published in Ocular Immunology and Inflammation, 2022
Carlos Cuadros Sánchez, Cristina Sacristán Egüen, Raquel Gutierrez-Ezquerro, Lena Giralt-Peret, Alex Fonollosa
On examination, the corrected distant visual acuity (CDVA) of the right eye was 20/32. In his left eye (OS), he did not present alterations in the anterior segment, with a CDVA of 20/20 and the IOP was 12 mmHg in OU. In the right eye funduscopy, optic disc edema, vascular tortuosity and hemorrhages were observed in 4 quadrants, no vitritis or sheathing was observed (Figure 1). He did not present alterations in the left eye. Optical coherence tomography (OCT) was performed, showing cystoid macular edema with subretinal fluid and a central thickness of 585 μm (Figure 2a). No evidence of paracentral acute middle maculopathy (PAMM), or acute macular neuroretinopathy (AMN) was found. A fluorescein angiography was also performed, which ruled out the existence of areas of ischemia and showed hyperfluorescence due to optic disc leakage and multiple hypofluorescent lesions corresponding to hemorrhages (Figure 3). The patient was diagnosed with non-ischemic central retinal vein occlusion of the right eye.
The Spectrum of Ocular Manifestations in Patients with Waldenström’s Macroglobulinemia
Published in Ocular Immunology and Inflammation, 2022
Rosanna Dammacco, Walter Lisch, Tero T. Kivelä, Evangelos Terpos, Efstathios Kastritis, Dario Sisto, Alberto Mavilio, Roberto Ria, Giovanni Alessio, Angelo Vacca, Franco Dammacco
A central retinal vein occlusion with secondary macular edema was diagnosed in the left eye of patient #11. As vascular endothelial growth factor-A (VEGF-A) is an important regulator of angiogenesis and therefore an anti-angiogenic target in retinal diseases,34 the patient was treated with ranibizumab (Lucentis®). Intravitreal injection of 0.5 mg ranibizumab monthly for three consecutive months resulted in a clinically meaningful gain in BCVA from baseline. After no response to six cycles of R-CD, the patient was switched to an R-CHOP regimen, which led to a complete response that was maintained for 3 years. A subsequent relapse was treated with the same R-CHOP regimen and induced a durable very good partial response, maintained until the end of follow-up. The ophthalmological improvement remained unchanged.
A review of risk factors for retinal vein occlusions
Published in Expert Review of Cardiovascular Therapy, 2022
Marie Ørskov, Henrik Vorum, Torben Bjerregaard Larsen, Nanna Vestergaard, Gregory Y. H. Lip, Toke Bek, Flemming Skjøth
The pathogenic mechanism of retinal vein occlusion is not fully characterized. Various theories for both branch retinal vein occlusion and central retinal vein occlusion with both similarities and differences have been described. A similarity between some of the theories, is the contribution of atherosclerosis to the development of retinal vein occlusion [5,6]. The central retinal vein and the central retinal artery share the adventitial sheath within the lamina cribrosa. Similarly, the branch retinal veins and the branch retinal arteries share a common adventitial sheath at the arteriovenous crossings. Therefore, one theory is, that if the retinal arteries become stiff and rigid due to localized atherosclerosis, they can obstruct the retinal veins by compression [5,7–13]. This theory has been challenged by a study investigating the lumen of the occluded retinal vein, where no signs of compression of the vein was determined [14]. Another theory suggests that the veins of the retina are specifically exposed to thrombosis formation due to the gradient between the vascular pressure and the intraocular pressure. Changes in the pressure gradient may cause partial collapse of the vein either in a branch retinal vein or in the entrance to the eye in the central retinal vein, making it susceptible to thrombosis formation. Initiation of thrombosis formation could be caused by the closely passing retinal artery, either by turbulence or changes in the biochemical environment resulting from changes caused by systemic atherosclerosis [15–22].