Experimental retinal vascular occlusion II (original) (raw)
Related papers
Archives of Ophthalmology, 2000
To investigate the significance of optic nerve head swelling (ONHS) in relation to the pattern of vascular nonperfusion, visual acuity (VA), and demographic profile in retinal venous occlusions (RVOs) occurring within the optic nerve. Methods: Cases of RVO occurring within the optic nerve were divided on the basis of the presence (105 cases) or absence (163 cases) of ONHS. This division was performed by examining the color stereo fundus photographs in conditions masked from other clinical parameters. Duration of symptoms before assessment, age, and sex distributions were compared. The vein involved was identified, and the occlusion was confirmed to have occurred within the optic nerve by observing that the vein pierced the lamina cribrosa as a dilated vein. Fluorescein angiographs were examined, and the extent of vascular nonperfusion in the macula and peripheral retina was quantified from grade 1 to grade 4. The extent of break in the perifoveal capillary arcade was graded as 0, less than or equal to 90°, and greater than 90°. Bestcorrected VA was assessed using the Snellen chart. Results: The 2 groups were comparable in terms of the duration of the symptoms before examination. The mean age was significantly younger in the group with ONHS (58.3 vs 65.1 years, PϽ.001). Age distribution by sex demonstrated a higher proportion of men younger than 50 years in the ONHS group (19.1% vs 8.6%, P=.01). The group without ONHS involved the papillary vein more frequently (31.3% vs 17.1%, P=.01). The respective proportions of grade 1, 2, 3, and 4 vascular nonperfusion in the macula were 90.5%, 9.5%, 0%, and 0% in the ONHS group, and 62.6%, 14.7%, 13.5%, and 9.2% in the group without ONHS (PϽ.001). The corresponding proportions for the peripheral retina were 90.4%, 8.7%, 0%, and 1.0% in the ONHS group, and 62.7%, 13.0%, 18.0%, and 6.2% in the group without ONHS (PϽ.001). In 64.6% of cases with ONHS and 42.9% of cases without, the perifoveal arcade was intact. A break greater than 90°in the perifoveal arcade was present in 12.5% of cases with and 23.6% of cases without ONHS (P=.004). The median VA was significantly better in the ONHS group (6/24 vs 6/48, P =.005). Conclusions: The RVOs occurring within the optic nerve can be subdivided into 2 distinct groups on the basis of ONHS. The presence of ONHS is associated with younger age, less severe vascular nonperfusion, and better VA. This is consistent with a retrocribrosal site of occlusion, which has access to the pial plexus that can provide collateral channels for retinal venous drainage.
Graefe's Archive for Clinical and Experimental Ophthalmology, 2008
Background Retinal vein occlusion (RVO) is the second leading cause of vascular eye disease. Currently there is no definite treatment for this condition. Animal models could be potentially helpful in developing new treatments; however, it is essential to understand the differences these models may have with human RVO. The aim of our study was to examine the course of experimentally created retinal vein occlusion (RVO) in rabbits. Methods Twenty-nine pigmented rabbits were included in the study. RVO was created in all using an argon green laser following intravenous injection of Rose Bengal. A laser was applied to all major veins at the optic disc margin to mimic central retinal vein occlusion. Animals were followed-up for a maximum of 2 months. Results Immediately following laser application, blood flow ceased or the flow was extremely slow in the retinal veins in all cases. At day 2 post laser, 86% showed significant retinal hemorrhages. On FA, no retinal blood flow was observed in the eye (neither arteries nor veins) in the majority of rabbits. Between weeks 1 and 3, laser sites reopened and partial or complete revascularization of both retinal arteries and veins occurred; however, the vascular pattern was abnormal. Conclusions RVO in rabbits has a different course than in human and it can be classified into three stages. At stage 1 (the first few days after laser photothrombosis), there is a retrograde propagation of the blood clot in the retinal veins that extends to the retinal arteries and choriocapillaries. As a result, there is no retinal blood flow at this stage in most cases. At stage 2 (between weeks 1 and 3), partial or complete revascularization occurs but the vessels have an abnormal pattern. At stage 3 (after week 3) no significant change takes place. Keywords Central retinal vein occlusion . Branch retinal vein occlusion . Rabbit . CRVO . BRVO . RVO . Laser photothrombosis . Rabbit vein occlusion
Bilateral Acute Retinal Necrosis
Archives of Ophthalmology, 1982
Four patients who experienced the sudden onset of anterior uveitis with large keratic precipitates and dense vitreous opacities developed confluent yellow-white swellings and exudates in the peripheral retina and sheathing and obliteration of retinal arteries. After absorption of the exudates, atrophic patches in the peripheral retina and a funnelshaped retinal detachment with many tears appeared. Angiograms showed retinal edema, fluorescein leakage from the choroid in the affected areas, and perivasculitis of the retinal arteries. Although treatment seemed unable to alter the course of the disease, in one case the retina reattached after vitrectomy and filling of the vitreous space with silicone oil. Histopathologic studies disclosed extensive atrophy and degeneration of the outer retinal layers and pigment epithelium and occlusion of the retinal vessels. An infection may trigger the uveitis, leading to an autoimmune sensitization against rods and cones that causes severe local immune-complex disease and retinal vasculitis.
Central Retinal Artery Occlusion: Acute Management and Treatment
Current Ophthalmology Reports, 2017
Purpose of Review-This review will seek to answer if advances in ophthalmic imaging and evolution of treatment modalities have shed further light on the epidemiology, pathophysiology, diagnosis, and acute management of acute CRAO. Recent Findings-Imaging characteristics of acute CRAO have been further characterized with the use of fluorescein angiography, optical coherence tomography (OCT), OCT-angiography, and indocyanine-green angiography. Layer segmentation of OCT imaging has found inner retinal layer hyper-reflectivity to be a common finding in acute CRAO. Non-invasive therapies, fibrinolytic delivery, and surgical interventions for acute CRAO have been further evaluated as potential management tools. Summary-A large body of literature reports very inconsistent treatment success with a wide variety of modalities. Currently, there is no clear evidence supporting the use of fibrinolytics in acute CRAO. Large, multicenter, randomized control trials are necessary to elucidate the role of the various acute treatment options in the management of CRAO.
Molecular and histological changes following central retinal artery occlusion in a mouse model
Experimental Eye Research, 2008
The aim of this study was to characterize the molecular and histological changes that occur in the retina following central retinal artery occlusion (CRAO) in a mouse model. CRAO was induced in 60 mice by laser photoactivation of intravenously injected rose bengal. Mice were sacrificed at 3, 6, 12, and 24 h and 7 and 21 days after CRAO induction for molecular analysis (5-13 mice/time point) and histological and apoptosis studies (3-4 mice/time point). Fundus examination and fluorescein angiography were also performed at various points. Retinal mRNA was analyzed for expression of T-cell antigen 1 (Thy-1), vascular endothelial growth factor (VEGF), heme oxygenase-1 (HO-1), and hypoxia-induced factor 1a (HIF-1a) using real-time polymerase chain reaction. The results showed that at 6-24 h following CRAO induction, the retina was edematous, with interrupted blood perfusion. Fluorescein angiography showed reperfusion at 6 h, and TdT-mediated dUTP nick end-labeling (TUNEL) assay revealed an increase in apoptotic cells in the first 24 h. On histological sections, nuclear loss in the inner retinal layers was maximal on day 21. Thy-1 expression decreased to 30% of baseline (P 0.002). VEGF expression increased in the first 3 h and gradually decreased thereafter, reaching 75% of baseline on day 21 (P 0.005). HO-1 was upregulated at all time points, with a peak at 12 h. No change was noted in HIF-1a expression at any time. In conclusion, CRAO in mice causes cell apoptosis in the inner layers of the retina, with a significant cell loss and a decrease in Thy-1 expression by 21 days. These changes are accompanied by a rise in expression of the ischemia-related protein HO-1 to a peak at 12 h, with levels remaining above control values at day 21. Given the similarity of the mouse model to human CRAO, these findings may have implications for the future clinical management of CRAO.
Current endovascular treatment options for central retinal arterial occlusion: A review
2014
C entral retinal artery occlusion (CRAO) is an ophthalmological emergency that can result in complete blindness in the affected eye if untreated. 3,5,6, 17,29,38,41,42,45 It is a result of sudden cessation of circulation to the inner retinal layer, which is considered to be a part of the CNS. This condition was first described in 1859 by Albrecht von Graefe, a famous German ophthalmologist known for his contributions in glaucoma and cataract treatment. 44 Since then, there has been an abundant accumulation of literature regarding the disease. Although the pathophysiological features of CRAO are well described in the literature, the natural history of this disease is poorly understood. Prolonged retinal ischemia is usually irreversible, suggesting a grim prognosis if the occlusion is not corrected in a timely manner. 38 In a matter of hours cellular hypoxia will ensue, with subsequent necrosis if circulation is not restored. The central retinal artery is usually occluded by a thrombotic embolus (of internal carotid artery or cardiac origin, 15.5% of cases); a calcified embolus (commonly of diseased cardiac valve origin, 10.5% of cases); or cholesterol embolus (74.5% of cases) (Table 1). 2,27,32 Other causes include sudden narrowing of the arterial wall (hemorrhage into an atheromatous plaque) and inflammatory processes (arteritic CRAO) secondary to temporal arteritis. 17 There is a high association of CRAO with atherosclerosis, diabetes, and systemic hypertension. 16 Epidemiology, Etiology, and Presentation The true incidence of CRAO in the population is unknown. One report estimated CRAO to occur in 1 per 10,000 outpatient visits. 10 The department of ophthalmology at the Western Galilee-Nahariya Medical Center in Nahariya, Israel, estimated an incidence of acute CRAO (with a less than 48-hour onset) at that institution to be approximately 0.85 per 100,000 per year or 1.13 per 10,000 outpatient visits. 38 Of these patients, 1%-2% present with bilateral involvement. Men are more frequently affected than are women, and the average age at presentation is in the early 60s, with rare cases as early as in the 30s. 1,38,40,42 Patients suffering from central retinal artery embolism have a 56% mortality rate over 9 years, compared with 27% for age-matched individuals without emboli. 18 Life expectancy is 5.5 years postdiagnosis for patients with CRAO compared with 15.4 years for age-matched individuals without CRAO. Diagnosis is usually made based on clinical history and physical examination. Ninety percent of patients present with a complaint of acute, persistent, painless loss of vision. Some patients may report a history of amaurosis fugax lasting anywhere from seconds to several hours. Ophthalmoscopic examination may reveal diminished blood vasculature in the retina, retinal edema, pale optic disc, and a cherry red spot. Approximately 18.7% of the
Cilioretinal arteries and collateral vessels after occlusion of central retinal artery
Vojnosanitetski pregled, 2016
Background/Aim. Central retinal artery occlusion (CRAO) is a disease of the eye where the flow of blood through the central retinal artery is blocked. It causes sudden, painless, unilateral and usually severe vision loss. The aim of our study was to examine significance of cilioretinal artery on collateral and neovasculatization development after occlusion of the central retinal artery. Methods. This study retrospectively reviewed all fluorescein angiography (FA) cases with confirmed CRAO and presenting, one or more, cilioretinal arteries on initial examination. The study included patients referred to the Clinic of Ophthalmology, Clinical Center Kragujevac for the examination in the period from January 2010 to January 2015. Ten eyes of 10 patients with confirmed CRAO and existing cilioretinal artery on initial examination were found and analyzed in this study. Results. This study included 10 (6 males and 4 females) patients from 50 to 76 years old (mean 66.3 ? 10.078 years). Visual ...