Choroidal Neovascularization: Function, Role & Diseases

What is choroidal neovascularization (CNV)? What is its purpose and

In which diseases does it occur? A brief overview follows in this article.

What is choroidal neovascularization?

Choroidal neovascularization (CNV) is an attempt by the body to bypass an undersupply of oxygen and nutrients to the retina. To do this, the body forms more small blood vessels in the eye. They arise from either the choroid or the choriocapillaris, a network of a multitude of small blood vessels within the large choroidal vessels and Bruch’s membrane.

Function and purpose

Choroidal neovascularization (CNV) is an attempt by the body to circumvent an undersupply of oxygen and nutrients to the retina. The yellow spot of the retina, the macula, has a high content of yellow macular pigment, which is a complementary color that provides natural protection from high-energy UV light and blue light for the retina. The macula is the most metabolically active area in the human body – and it does so throughout our lives without us even realizing it. A high throughput of energy and nutrients takes place. Via the arteries, oxygen and nutrients are provided for the visual cycle. Metabolic waste products and carbon dioxide are removed via the veins. The photoreceptor cells – rods and cones – are erect with one end in the retinal pigment epithelium, which is connected to the choroid via the selectively permeable blood-retinal barrier. In a healthy eye, there is a balance between supply and disposal of metabolic products. In the course of the human aging process, the network of choriocapillaris is no longer as well developed: The area of the central macula is then no longer as well supplied with oxygen and nutrients. To compensate for this, the body initiates choroidal neovascularization. However, this can also take a pathological course. A number of diseases can also result in a lack of oxygen (hypoxia) in the retina. As a result, the VEGF factor is released, a growth factor that accelerates the formation of new vessels to correct the undersupply of the photoreceptors in the retina. These newly formed vessels always entail that they are inaccurately built and their vessel walls are fragile. This leads to edema and bleeding in the retina. This is the reason for distorted vision. The visual disorder can be easily detected with the help of an Amsler grid. For this purpose, the center of a grid field is fixed with one eye

while the other eye is covered. If the lines are curved, wavy, or distorted, this is a sign of macular disease, behind which CNV may lie. If areas of vision have already failed, scotomas (visual field loss) show up as white or gray spots. If the visual fossa is affected, visual acuity drops rapidly. If only a small area is affected, there are reading difficulties: Individual letters are incomplete, jump or are distorted. Recognizing faces is difficult or becomes impossible due to the central visual field loss in later stages.

Diseases and medical conditions

Age-related macular degeneration (AMD) occurs in two forms. In dry AMD, the photoreceptors of the central macula starve without the release of growth factors. The precursor to AMD is an accumulation of drusen, which are collections of metabolic waste products, because the retinal pigment epithelium is no longer up to the task of disposing of these products. The final stage of dry AMD is geographic atrophy: the photoreceptor layer is then no longer present. The retinal pigment epithelium no longer has any function at this site. The tissue has thinned out. The choroid now shows more clearly. If the VEGF factor is expressed, fragile blood vessels are produced in CNV to provide a substitute supply of oxygen and nutrients to the photoreceptor cells. If these leak, edema develops, which can be seen as a thickening of the retina in cross-section on optical coherence tomography (OCT). Visual acuity decreases rapidly. The therapeutic goal is to drain the edema. Several methods are available for this purpose. In addition to oral agents with high side effects, there are agents administered directly into the eye with an injection. The precursor was sclerotherapy by laser (Macugen, photodynamic therapy – PDT). In pathologic myopia, retinal changes are seen.The overlong eyeball permanently stretches the retina. This increases the risks of retinal detachment and twilight vision loss due to degeneration in the outer retina. The overstretching leads to a thinner macula. The blood vessels of the choroid are also stretched due to the stretching. The retinal pigment epithelium is also stretched. This stretching can lead to lacquer cracks, which the ophthalmologist sees as fine branched lines when viewing with an ophthalmoscope. At the corresponding location, a tear has occurred in Bruch’s membrane and in the retinal pigment epithelium. At the same time, hemorrhage has occurred below the retina. The hemorrhage results from rapidly grown vessels of a CNV at this tear site. OCT shows a retinal edema. The final stage is a Fuchs spot as a slightly raised and pigmented scar in the visual fossa with significantly reduced visual acuity. CNV can also develop from retinal choroiditis. Toxoplasmosis can develop foci of inflammation on the retina. Even after the inflammation has resolved, CNV can develop from these scars. The same is true with uveitis.