Occlusion Of Retinal Arterioles Research Articles

Retinal vasculopathy following varicella zoster virus infection.

Varicella zoster virus (VZV) ocular infection can manifest purely as a vasculopathy that leads to retinal arteriole occlusion, without any retinitis or vasculitis. This review summarizes our current knowledge of such VZV ocular infection phenotype, incorporating initial descriptions from 1988. We describe the pathogenesis and VZV's manifestations in the retina using fundus photography, fundus fluorescein angiography, optical coherence tomography (OCT) and optical coherence tomography angiography (OCTA). Laboratory investigations, diagnostic procedures, prognoses, and treatment options are also being reviewed. Ten case reports where VZV retinal vasculopathy was the primary feature observed after varicella or zoster rash are described. The retinal arteriole, cilioretinal artery, branches of retinal artery, central retinal artery and ophthalmic artery were found to be areas of more rarely affected, neither in the form of vasculitis nor retinitis. Diagnosis is typically made from positive polymerase chain reaction (PCR) for VZV from extracted intraocular fluid or positive serum or cerebrospinal fluid (CSF) anti-VZV immunoglobulin G antibody in the context of compatible ocular findings. In addition, retinal vasculopathy occurring in the setting of confirmed varicella or zoster rashes could be considered potentially pathognomonic. Pathological concepts, including direct VZV infection of affected tissue, persistent inflammation, and/or virus-induced hypercoagulability are also discussed. VZV may produce a wide spectrum of ocular manifestations with isolated VZV retinal vasculopathy being a rarer presentation. A prompt diagnosis followed by an early treatment of systemic acyclovir with or without corticosteroids is the mainstay of treatment.

Retinal Arteriolar Occlusions and Exudative Retinal Detachments in Malignant Hypertension: More Than Meets the Eye

Malignant hypertension is macrovascular and microvascular endothelial injury responsible for multiple organ damage. Considering the anatomical and functional homologies between the posterior pole of the eye and the kidney, ophthalmological explorations may inform clinicians on the mechanisms underpinning concurrent kidney injury in this condition. More specifically, we investigated whether the wall-to-lumen ratio (WLR) of retinal arterioles measured by adaptive optics ophthalmoscopy could be correlated to WLR of kidney arterioles as determined by pathology. We sought to estimate the incidence of retinal arteriole occlusion a supposedly uncommon complication of malignant hypertension. All patients hospitalized in our renal Intensive Care Unit for malignant hypertension between 2016 and 2019 were referred to ophthalmological examinations. Twenty-seven patients were included. Median retinal WLR was 0.39 [0.31-0.47] and was correlated with initial systolic (r = 0.56, P = 0.003) and mean blood pressure (r = 0.46, P = 0.02) upon admission. The retinal WLR was not correlated to renal pathological findings, as assessed by juxtaglomerular WLR (r = 0.38, P = 0.2), ratio of glomerulosclerosis (r = -0.39, P = 0.2), or tubulointerstitial fibrosis (r = -0.45, P = 0.08). Retinal WLR was not associated with neurological or cardiovascular end-organ damage. Branch retinal artery occlusion was detected in 18.5% of patients and exudative retinal detachment (ERD) in 29.6% of patients, without any significant correlation with canonical signs of retinal hypertension including optic disc swelling. In the setting of malignant hypertension, we failed to demonstrate a significant relationship between WLR and other meaningful end-organ injuries. However, branch retinal artery occlusion and ERD may have been hitherto underestimated.

Branch retinal artery occlusion associated with photodynamic therapy in a circumscribed choroidal haemangioma

We report a case with retinal arteriole occlusion after a single photodynamic therapy (PDT). A 33-year-old man presented with decreased visual acuity of the right eye, 20/200, for four months. Diagnosed as circumscribed choroidal haemangioma (CCH), he was treated with the PDT. Specifically, 6 mg/m(2) of verteporfin was administered intravenously in 10 min. Laser treatment was performed 15 min after the infusion with an exposure of 75 J/cm(2) for 125 s. The patient was followed up a week later and then every month for 5 months. Complaining about central visual field defect two days post treatment, he was diagnosed with inferior macular artery occlusion with FA. After three months further treatment, the tumor regressed completely but local retinal atrophy was observed. The best corrected visual acuity (BCVA) was 20/30 with visual field defect. Following this, extensive blood tests were performed, revealing no abnormality. Our result indicates that under certain conditions infarction of retinal arterioles can develop following PDT.

Superselective Intraophthalmic Artery Chemotherapy in a Nonhuman Primate Model

We describe the histopathologic findings in a nonhuman primate (NHP) model of superselective intraophthalmic artery chemotherapy (SSIOAC), detailing ocular and orbital vascular adverse effects. To further document, using comprehensive ocular and orbital histopathology, previously reported toxic effects observed with real-time ophthalmoscopy during SSIOAC in a NHP model. Comparative interventional case series. Preclinical trial approved under the guidelines of the Institutional Animal Care and Utilization committee. Six adult male rhesus macaques (Macacca mulatta). The right eye of each NHP was treated with 3 cycles of SSIOAC using either melphalan (5 mg/30 mL) or carboplatin (30 mg/30 mL). Both eyes in each animal were enucleated 6 hours after the final procedure, before euthanasia and formalin perfusion of the NHP; we then performed orbital dissection of the arterial vasculature and optic nerves. Histopathologic examination of the eyes, optic nerves, and orbital vessels of the 6 treated NHPs. We found leukostasis with retinal arteriole occlusion in all treated eyes. Retinal endothelial cells stained positive for 2 inflammatory markers, intercellular adhesion molecule 1 and interleukin 8. Transmission electron microscopy revealed occlusion of the retinal vessels with ultrastructural changes in the endothelial cells and surrounding pericytes. Additional findings included nerve fiber layer infarcts, central retinal artery thrombosis, hypertrophy and occlusion of choroidal arteries with disruption of the internal elastic lamina, patchy choroidal inflammation, and birefringent intravascular foreign bodies. Orbital findings included ophthalmic artery and central retinal artery wall dissection, fracturing of the internal elastic lamina, intimal hyperplasia, and eyelid vessel damage. Optic nerves displayed hemorrhage, leukostasis, and foreign body crystallization. Control eyes, optic nerves, and orbital vessels were normal. Histopathologic examination of our nonhuman primate model for SSIOAC revealed significant toxic effects in the ocular and orbital vasculature. These findings substantiate previous observations with real-time retinal imaging and parallel reported vascular toxic effects in children with retinoblastoma treated with SSIOAC.

Takayasu disease on the centenary of its discovery

Takayasu disease was first reported in 1908 by Mikito Takayasu as "a case of peculiar changes in the central retinal vessels." Because in these patients the pulse of the radial artery is impalpable, investigations focusing on the ischemic symptoms of the upper body were conducted. In 1948, Shimizu and Sano named this pathological condition "pulseless disease." Since then, the lesions of Takayasu disease have been detected not only in the aortic arch and its main branches but also in various vessels, including the abdominal aorta and renal arteries. The ocular symptoms of Takayasu disease are considered to be due to ischemia in the retina and choroid. The typical wreath-like arteriovenous anastomosis around the disc reported by Takayasu is observed at a relatively late stage of the disease. The characteristic fundus findings of Takayasu disease include tortuosity and dilatation of the central retinal artery and vein, retinal arteriovenous anastomosis, prominent retinal vasculature, microaneurysms in the capillaries, occlusion of retinal arterioles, soft exudate, choked disc, and optic atrophy. Fluorescein angiography reveals retinal microaneurysms, sludging, slower blood flow, dilatation of retinal vessels, leakage of fluorescence dye due to increased vascular permeability, and arteriovenous anastomosis. Arteriovenous anastomosis initially appears in the periphery at the early stage, and in the arteriovenous crossing at the advanced stage. Systemic administration of corticosteroids is required to prevent vascular stenosis during the early stages of Takayasu disease. Reconstruction of the carotid artery may improve subjective symptoms and fundus findings.

Transpupillary thermotherapy for age-related macular degeneration: Principles and techniques

Transpupillary thermotherapy (TTT) is a subthreshold, low irradiance, long exposure duration, large spot size, infrared diode laser protocol. Retinal temperature increases in TTT for choroidal neovascularization (CNV) are substantially lower than those in conventional short-pulse photocoagulation, but they are maintained for 60 seconds to achieve therapeutic results. Treatment power is adjusted for retinal lesion size, chorioretinal pigmentation, macular elevation and media clarity. TTT uses 810-nm diode laser infrared radiation, which has no significant retinal phototoxicity. A parfocal laser delivery system is required to assure uniformity of irradiance across large diameter treatment spots. Relative contraindications for TTT include dense subretinal hemorrhage, prior focal photocoagulation and serous RPE detachment. Adverse events are rare, and include decreased vision and retinal arteriole occlusion. Randomized, prospective multi-center trials are underway to compare the results of TTT for occult CNV in age-related macular degeneration to the natural history of the disorder. Imaging, electrophysiologic or thermometric techniques may ultimately provide intra-operative or post-operative monitoring to assure the adequacy of TTT for CNV, despite the absence of ophthalmoscopically visible lesions.

Acute vascular occlusion of the eye fundus: ocular and general evaluation. General treatment plan

Occlusion of retinal arterioles and veins and acute papillitis are often local manifestations of systemic disease. Treatment should start as soon as the diagnosis is made. At the same time the ocular lesions should be assessed and the local and systemic risk factors sought. Identified risk factors should be treated immediately if possible. The primary aim is to reestablish perfusion in the occluded vessels in order to limit the extent of lesions and to restore function. In practice, intervention is often too late. Subsequent treatment aims at consolidating the result, and may take a year; relapse should be avoided by treatment of the risk factors.