Choroidal Neovascularization: OCT Angiography Findings

From EyeWiki


Type 1 CNV. Type 1 neovascular lesion is located below the RPE as seen in the B-scan frame. In the OCT-A frame, a neovascular coralliform network is observed which emanates from the choroidal vasculature and extends to the sub-RPE space.

Choroidal neovascularization (CNV) is part of the spectrum of exudative age-related macular degeneration (AMD) that consists of an abnormal growth of vessels from the choroidal vasculature to the neurosensory retina through the Bruch's membrane. Leakage of retinal edema and hemorrhage from CNV in exudative AMD threatens visual acuity.


Etiology of CNV is multifactorial. Alterations in Bruch's membrane, migration of macrophages and production of vascular endothelium growth factor (VEGF), play an important role in the development of this disease.

Risk Factors

Type 2 CNV. In B-scan and OCT-A, a neovascular lesion is identified that extends from the choroidal vessels through the Bruch's membrane and RPE and grows into the subretinal space. The En Face image shows a change in color in macula secondary to edema and serous detachment of the retina.

The incidence and progression of AMD are related to age and genetic factors. With aging, the lysosomal activity for the degradation of external segments of photoreceptors decreases. This leads to subsequent accumulation of lipofuscin, which affects the normal function of the RPE. Another important risk factor for the development of CNV is the presence of large, confluent soft drusen. . Oxidative stress may play an important role in AMD. Several modifiable risk factors have been identified, including quitting smoking, dietary intake of omega-3 fatty acids and vegetables and fruit with antioxidants including lutein and zeaxanthin, as well as, exercise, and maintaining a healthy weight.


Alterations in the normal transport of metabolites, ions and water through Bruch's membrane in AMD, alter the nutrition and stability of retinal pigment epithelium (RPE) from choriocapillaris and the transport of waste out from the neurosensory retina. Hypoxia leads to VEGF being released by RPE that initiates a cascade of angiogenic responses at the level of the choroidal endothelium. Bruch´s membrane damage is required to allow the passage of abnormal neovascular vessels from the choroidal vasculature through the breaks in Bruch’s membrane to the retina. This impairment is part of the pathological course of AMD.


Histologically, neovascular membranes are classified into:

Type 1, when the neovascular membrane is located below the RPE.

Type 2, passes through the RPE and is located above the RPE in the subretinal space. This is related to angiographic classification: type 1 corresponds to hidden CNV and type 2 corresponds to classic CNV. Type 3 is defined as Retinal Angiomatous Proliferation (RAP), which corresponds to neovascularization that develops within the neurosensory retina.

Clinical findings

Type 3 CNV.  An intraretinal neovascular lesion is observed. The color photo identifies typical punctate hemorrhages. The OCT B-scan shows retinal edema without disruption of Bruch's membrane or RPE. OCT-A depicts an anastomosis originating in the neurosensory retina.

In the presence of CNV, the patient experiences an acute decrease in visual acuity, relative scotoma and metamorphopsia. The retinal examination shows a grayish macular lesion associated with subretinal fluid, cystoid macular edema, exudation and hemorrhages.

Diagnostic procedures

OCT ANGIOGRAPHY OCT ANGIOGRAPHY: En face OCT angiography (OCTA) is a new technology that has a great ability to show detailed retinal structures and chorioretinal microcirculation without contrast medium or without invasive means. It uses an optimized long wavelength (1,050nm), which can penetarte deeper layers of the eye and can traverse opacities of media such as cataracts, hemorrhages, vitreous opacities, pigment, among others. It can also configure three-dimensional analysis of the chorioretinal and vascular lesions. Type 1 CNV is observed by OCT-A as a neovascular coralliform complex with afferent vessel, originating in the choroid. The type 2 CNV is visualized as a neovascular network that grows from the choroid vasculature, traverses the RPE-Bruch's membrane complex into the subretinal space. Type 3 CNV is clinically seen as tiny intra- and subretinal hemorrhages that correlate on OCT-A to an intraretinal anastomosis originating in the deep capillary plexus of the retina.


Taking into account the numerous recent studies on the treatment of CNV in AMD, it has been shown that antiangiogenic therapy shows the best result both histologically with the regression of the neovascular lesion and functionally with improvement of the visual acuity. Although the treatment is the same for all types of CNV, it is important to differentiate them, since they do not all respond identically and some of them have a higher rate of recurrence.


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