Choroidal Neovascularization: OCT Angiography Findings

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Disease

Type 1 CNV. As seen in the image of CNV type 1 is a neovascular lesion that is located below the RPE observable in the B-scan. In the OCT-A a neovascular coralliform network is observed. Comes from the choroidal vasculature and extends below de RPE.

Choroidal neovascularization (CNV) is part of the spectrum of age-related macular degeneration (AMD) consisting of the abnormal growth of vessels from the choroidal vasculature to the neurosensory retina through the Bruch's membrane. Exudative AMD is the main complication that threatens visual acuity.

Etiology

CNV is a multifactorial lesion, produced due to numerous stimuli. Alterations in Bruch's membrane, involvement of macrophages and vascular endothelium growth factor (VEGF), take the main role for 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 and EPR membranes, compromising the external retina. In B-scan and OCT-A, a neovascular lesion is identified that extends from the choroidal vessels through the Bruch and EPR membranes, compromising the external retina. In the image En Face shows a change of color in the external retina 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 a 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 soft drusen as opposed to hard ones.

Several modifiable risk factors have been identified, including 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.

Pathophysiology

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. VEGF is then released by RPE as a stress signal and hypoxia that initiates a cascade of angiogenic responses at the choroidal endothelium level. Bruch´s membrane damage is required to allow neovascular passage through it from the choroidal vasculature to the retina. This impairment is part of the pathological course of AMD

Classification

Histologically, neovascular membranes are classified into: Type 1, when the neovascular membrane is located below the RPE Type 2, as it passes through the RPE, compromising the neurosensory retina

This has been related to angiographic classification: type 1 corresponds to hidden CNV and type 2 corresponds to classic CNV.

Type 3 has been defined as RAP (Retinal Angiomatous Proliferation), which corresponds to neovascularization developed within the neurosensory retina.

Clinical findings

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

In the presence of CNV, the patient refers a sudden decrease in visual acuity and metamorphopsia. The ophthalmologic examination shows a grayish macular lesion associated with subretinal fluid, exudation and hemorrhages.

Diagnostic procedures

OCT ANGIOGRAPHY En face OCT angiography (OCTA) is a new technology that has a great ability to detail retinal structures and chorioretinal microcirculation without contrast medium or without invasive means. It uses an optimized long wavelength (1,050nm), which achieves a better penetration of 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, originated in the choroid. The type 2 CNV is visualized as a neovascular network that is born from the choroid traverses the EPR-MB complex to compromise the external retina. Type 3 is identified as an intra- and subretinal bleeding correlated in OCT-A with an intraretinal anastomosis originating in the deep capillary plexus of the retina.

Treatment

Taking into account the numerous and recent studies on the treatment of CNV in AMD, it has been shown that antiangiogenic therapy is the one that has shown the best results both histologically with the regression of the neovascular lesion and functionally with the 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.

References

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