scholarly journals Aflibercept Treatment and Regimes in Macular Edema Secondary to Central Retinal Vein Occlusion

Central retinal vein occlusion (CRVO) is the most common vascular disease leading cause of vision loss after diabetic retinopathy (DR) and branch retinal vein occlusion (BRVO). The pathogenesis of CRVO involves a thrombus formation leading to increased retinal capillary pressure, increased vascular permeability, and possibly retinal neovascularization. Vision loss due to CRVO is commonly caused by macular edema. Multiple treatment modalities have been used to treat macular edema. Currently, the most common therapy modality used is intravitreal inhibition of vascular endothelial growth factor (VEGF). The three most widely used agents are aflibercept, bevacizumab, and ranibizumab. In addition, intraocular steroids can be used to treat macular edema. This review will briefly cover the treatment options and discuss in greater detail the efficacy and safety of aflibercept.

Central retinal vein occlusion (CRVO) is the second most common vascular disease leading cause of vision loss together with branch retinal vein occlusion (BRVO) after diabetic retinopathy (DR). Vision loss due to CRVO is commonly caused by macular edema and multiple treatment modalities have been used to treat macular edema. In clinical practice, VEGF inhibitors are now the first-line treatment offered to patients who have CRVO with macular edema. The two agents approved by the FDA for the treatment of macular edema are aflibercept and ranibizumab. Bevacizumab is another VEGF inhibitor that has been used off-label to treat macular edema. Several studies have demonstrated that bevacizumab is effective in improving vision and decreasing central macular thickness when used in patients with macular edema due to central retinal vein occlusions. In the current review, the treatment options will be evaluated briefly and the efficacy and safety of bevacizumab will be discussed in greater detail.


Central retinal vein occlusion (CRVO) is a common and dramatic cause of sudden, painless, and unilateral visual loss. The vast majority of vision loss associated with CRVO results from the macular edema and neovascularization. The diagnosis is generally based upon the history and fundus examination. Common clinical evaluations include fluorescein angiography (FA) and optical coherence tomography (OCT). According to retinal perfusion status, CRVO is classified into two clinical types, and it is important to differentiate between the more common nonischemic type and the less common ischemic type. It is possible to detect the peripheral ischemic areas with wide-angle FA, while the perfusion status of the macula is evaluated by OCT angiography, which takes place in our daily practice.


Author(s):  
Alan D. Penman ◽  
Kimberly W. Crowder ◽  
William M. Watkins

The Standard Care vs. Corticosteroid for Retinal Vein Occlusion (SCORE-CRVO) Study was a randomized clinical trial comparing intravitreal triamcinolone to observation in eyes with vision loss associated with macular edema due to perfused (nonischemic) central retinal vein occlusion (CRVO). The results suggested that intravitreal triamcinolone in a 1-mg dose should be considered for up to 1 year, and possibly 2 years, in patients with vision loss associated with macular edema secondary to CRVO. The study was the first to establish an effective treatment for perfused CRVO. (Treatment with intravitreal anti–vascular endothelial growth factor [VEGF] agents has been shown to produce greater improvement in visual acuity and is now the standard of care.)


2020 ◽  
Vol 9 (11) ◽  
pp. 3457
Author(s):  
Hidetaka Noma ◽  
Kanako Yasuda ◽  
Masahiko Shimura

Central retinal vein occlusion (CRVO) causes macular edema and subsequent vision loss and is common in people with diseases such as arteriosclerosis and hypertension. Various treatments for CRVO-associated macular edema have been trialed, including laser photocoagulation, with unsatisfactory results. However, when the important pathogenic role of vascular endothelial growth factor (VEGF) in macular edema was identified, the treatment of CRVO was revolutionized by anti-VEGF therapy. However, despite the success of intraocular injection of anti-VEGF agents in many patients with CRVO, some patients continue to suffer from refractory or recurring edema. In addition, the expression of inflammatory cytokines increases over time, causing more severe inflammation and a condition that is increasingly resistant to anti-VEGF therapy. This indicates that the pathogenesis of macular edema in CRVO is more complex than originally thought and may involve factors or cytokines associated with inflammation and ischemia other than VEGF. CRVO is also associated with leukocyte abnormalities and a gradual reduction in retinal blood flow velocity, which increase the likelihood of it developing from the nonischemic type into the more severe ischemic type; in turn, this results in excessive VEGF expression and subsequent neovascular glaucoma. Here, we review the role of different factors and cytokines involved in CRVO pathogenesis and propose a mechanism that holds promise for the development of novel therapies.


2018 ◽  
Vol 3 (1) ◽  
pp. 45-48
Author(s):  
Omar Moinuddin ◽  
Matthew G. J. Trese ◽  
Cagri G. Besirli

Isolated retinal racemose hemangioma is a rare disorder that may lead to vision loss due to late complications, most commonly central retinal vein occlusion (CRVO). We describe the longitudinal clinical course using multimodal imaging of a 13-year-old girl diagnosed with CRVO and macular edema in the setting of isolated retinal racemose hemangioma treated with intravitreal antivascular endothelial growth factor.


Retinal vein occlusion (RVO) is the second most common vascular disease after diabetic retinopathy. Central retinal vein occlusion (CRVO) is less common than branched retinal vein occlusion. There are different aspects of the mechanisms underlying etiology and optimal treatment strategies in CRVO. There are various treatment modalities for CRVO including observation, systemic treatments, intravitreal agents, laser photocoagulation, fibrinolytic treatment, and surgical approaches. Despite most of the treatment strategies are directed at secondary complications of CRVO that affect vision including macular edema and retinal neovascularization, some treatment options also have the ability to create a bypass around the obstructed retinal vein and to decrease the raised venous hydrostatic pressure. The aim of this review is to describe the outcomes of surgical treatment modalities for CRVO.


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