Central Retinal Vein Occlusion
This is a [INAUDIBLE] lecture on central retinal vein occlusion. Center retinal vein occlusion affects men and women equally. It occurs predominantly in persons over the age of 65 years old and population based studies have reported the prevalence of central retinal vein occlusion at 0.1% to 0.4%.
CRVO is usually a unilateral disease but it is estimated that up to 7% of persons with CRVO may develop CRVO in the fellow eye within five years onset in the first eye. Patients often present with sudden, painless loss of vision, but they may also present with a history of gradual visual decline. They may correlate with a series less severe occlusions. Retinal hemorrhages, both superficial flame-shaped and deep blot-shaped hemorrhages, may be s seen in all four quadrants of the fundus with a dilated, tortuous retinal venous system. Optic nerve head swelling, cotton-wool spots, splinter hemorrhages, and macular oedema are present to varying degrees. Break through vitreous hemorrhage may also occur. With time, the extent of retinal hemorrhage may decrease or resolve completely with variable degrees of secondary retinal pigment epithelial alterations.
Macular edema often persist chronically. Epiretinal membranes may form. Optocillary shunt vessels, also known as optic disc collaterals may develop. Neovascularization of the disc or elsewhere may result in vitreous hemorrhage or tractional retinal detachment. Patients often preserve a poor visual acuity at onsets. In the CVOS study, these patients have only a 20% chance for improvement. Anterior-segment findings may include iris and/or angle neovascularization. Long-standing neovascularization of the iris or angles eventually lead to secondary angle closure from peripheral anterior synechiae formation known as neovascular glaucoma.
Neovascularization angles may develop without any neovascularization of the iris in 6% to 12% of eyes through central retinal vein occlusion. Nonperfused or ischemic central retinal vein occlusion demonstrates 10 or more disc areas of retinal capillary nonperfusion on fluorescein angiography. In eyes that are initially categorized as perfused, 10% developed neovascularization of the iris or angles compared to 5% of eyes initially characterized as nonperfused. 34% of initially perfused eyes convert to nonperfused status after three years. This is a fundus photograph of central retinal vein occlusion with excessive intraretinal hemorrhage. If a fundus fluorescein angiogram is performed in such an eye extensive blocking of fluorescein by the hemorrhages will preclude accurate determination of perfusion status. In this photograph below, optociliary shunt vessels, also known as collateral vessels, can be seen at the inferior border of the optic nerve head.
[INAUDIBLE] the pathogenesis of central retinal vein occlusion, within the retrolaminar portion of the optic nerve, the central retinal artery and vein are aligned parallel to each other in a common tissue sheath. The central retina artery and vein are naturally compressed as they cross through the rigid sieve-like openings in the lamina cribosa. These vessels may be subject to compression from mechanical stretching of the lamina as it increases intraocular pressure, which may cause a posterior bowing of the lamina and subsequent impingement of the central retinal vein. Hemodynamic alterations may also produce stagnant flow and subsequent thrombus formation in the central retinal vein. These alterations, also known as Virchow's triad, include diminished flow, increased blood viscosity, and an altered lumen wall.
Neovascularization of the anterior and posterior segment and severity of macular edema and modulated by growth factors released from the ischemic retina. These growth factors include vascular endothelial grow factor along with the other cytokines and growth factors which include interleukin-6 and -8, interferon-induced protein 10, monocyte chemoattractant protein 1, and platelet-derived growth factor. The risk factors and associations of central retinal vein occlusion includes systemic vascular diseases such as diabetes mellitus and hypertension, ocular diseases such as open angle glaucoma, ischemic optic neuropathy, hematologic alterations such as hyperviscosity syndromes and coagulation disorders, inflammatory autoimmune vasculitis such as SLE.
Medications such as oral contraceptives and diuretics may also predispose to a thrombotic state leading to central retinal vein occlusion. The degree of macular edema and retinal ischemia will determine treatment options and the follow up schedule. In terms of the history, the onset of occlusion and the systemic diseases are important. In the examination, visual acuity, pupillary reaction, and intraocular pressure are important to note.
Undilated [INAUDIBLE] examination is important to detect neovascularization of the iris or angles. Optical coherence tomography and fluorescein angiogram are helpful in evaluating and following the presence of macular edema and perfusion status. In general, systemic workup is not indicated in persons older than 60 years of age.
We've known systemic vascular risk factors for central retinal vein occlusion. Younger patients are more likely to have predisposing conditions resulting in thrombotic disease. A limited systemic workout may be considered in those with a prior occlusion in the fellow eye, prior systemic thrombotic disease, family history of thrombosis, or other symptoms suggestive of a hematologic or rheumatologic condition. This is a fundus photograph of an eye on the left side with central retinal vein occlusion which shows scattered retinal hemorrhages, venous tortuosity and engorgement as well as cotton-wool spots. The photograph on the right is a midphase fluorescein angiogram of the eye shown which demonstrates capillary nonperfusion involving the foveal center as well as the peripheries.
In terms of treatment of macular edema, laser photocoagulation has been shown in the CVOS study not to improve vision despite reduction of angiographic macular edema at 36 months. Intravitreal anti-vascular endothelial growth factor therapy is not the gold standard for the treatments of macular edema in patience with central retinal vein occlusion. In the CRUISE trial, monthly intravitreal injections of 0.3 milligrams or 0.5 milligrams ranibizumab was compared to sham-injected eyes for the treatment of macular edema after central retinal vein occlusion. In the 0.3 milligrams ranibizumab group, 46.2% of eyes and 47.7% of eyes in the 0.5 milligrams ranibizumab treated eyes gained more than or equals to 15 letters from baseline compared to only 16.9% in the sham group.
The use of intravitreal pharmacotherapy has replaced observation as the previous standard of care. Corticosteroid therapy is mainly a second line therapy for eyes with macular oedema not responding to antivascular endothelial growth factor. In the SCORE study, intravitreal triamcinolone acetonide has been shown to provide significant improvement in visual acuity compared to observation.
And in 2009, a sustained release intravitreal dexamethasone delivery system, Ozurdex, was approved for the treatment of macular edema secondary to CRVO. Use of corticosteroids is limited by the risk of cataract formation and elevated intraocular pressure. Laser photocoagulation is a gold standard for the treatment of ocular neovascularization. In the CVOS study, the efficacy of prompt PRP in eyes with nonperfused CRVO was compared to PRP application only when neovascularization of the iris and angles was detected. Neovascularization of the iris or angles developed in 20% of eyes that received prompt PRP compared to 34% of eyes that did not receive prompt PRP.
Prophylactic placement of PRP may be considered in eyes with non-perfused central retinal vein occlusion and who have risk factors for developing neovascularization of the iris or angles. These risk factors include male gender, short duration of CRVO, extensive retinal nonperfusion, and extensive retinal hemorrhage or in cases where frequent ophthalmologic follow up is not possible. Identification and treatment of systemic vascular risk factors are of paramount importance in individuals with CRVO. Thus, coordination with the internist is strongly recommended. Alternative treatments that have been described for central retinal vein occlusion include chorioretinal venous anastomosis, injection of tissue plasminogen activator, and radial optic neurotomy. Vitrectomy may be performed in eyes with non-clearing vitreous hemorrhage.
In conclusion, CRVO is a sight-threatening disease with significant ocular morbidity, including macular edema and ocular neovascularization. Intravitro antivascular endothelial growth factor has now replaced observation as the standard of care for the management of macular edema associated with CRVO. PRP is recommended in patients with non-profuse CRVO. Co-management with an internist to control underlying cardiovascular risk factors is crucial and consider further investigations in younger patients as well as patients without ischemic risk factors.
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